I
[vif)^s>, bA^^ '9^: (^
Control of Vegetation
on Utility and Roilfood
Rights-of-WQy
iO
\w
SEPl
\ \985
■sett*
CopV
Commonwealth of Massachusetts
Final Generic Environmental Impact Report
January 1985
HARRISON BIOTECH
Cambridge, Massachusetts
A GENERIC ENVIRONMENTAL IMPACT REPORT
ON
THE CONTROL OF VEGETATION
ON UTILITY AND RAILROAD RIGHTS-OF-WAY
IN THE
COMMONWEALTH OF MASSACHUSETTS
by
J. Harrison, President
HARRISON BIOTECH, INC.
for
DEPARTMENT OF FOOD AND AGRICULTURE
COMMONWEALTH OF MASSACHUSETTS
January 1985
PUBLICATION #13945-475-550-2-85-0. R.
Approved by: Daniel Carter, Purchasing Agent
ACKNOWLEDGEMENTS
Many individuals provided valuable assistance in the conduct of this
program. Carol Mishler, David Glaser, Richard Koske and Donald
Senechal provided particularly important contributions. The author is
also grateful to many individuals at Harvard University for information
and advice which they gave freely. Several Advisory Task Force
members also contributed in important ways to this report; Christopher
Davis, Esq., Rufin Van Bossuyt, and Jeff Taylor deserve special
commendation for their assistance. The production of the report
depended on the heroic efforts of Nan White, Maria Abate, and the
people at Wordsmith. Finally, the author thanks the staff of the Farlow
Herbarium of Harvard University for their encouragement and patient
support.
-11-
TABLE OF CONTENTS
ABOUT THIS REPORT 1
OVERVIEW 3
Historical practices 7
Vegetation control problems on rights-of-way 9
THE HERBICIDE ALTERNATIVE 11
Current practices 11
Herbicides covered in this report 13
Effects on public health 15
Potential for contamination of surface water and
ground water 31
Effect on non-target organisms 49
Minimizing the effects of herbicides 54
PHYSICAL ALTERNATIVE 57
Handcutting 57
Mechanical cutting 59
Fire 61
Other physical methods 63
BIOLOGICAL CONTROL 64
Control by natural enemies 64
Control by competition 66
Conclusions regarding biological
control on rights-of-way 71
INFORMATION REQUESTED BY REVIEWERS 72
EVALUATION OF ALTERNATIVES 98
Flexibility 98
Cost 101
Environmental impact 107
RECOMMENDATIONS 108
-ui-
APPENDIX I: SUPPLEMENTAL INFORMATION I-l
1. Legal Framework 1-3
2. Location of Public eind Private Wells 1-29
3. Biological Control: Additional Discussion 1-32
4. Methods for Marking Rights-Of-Way 1-45
5. Recommendations for Spill Clean Up 1-47
6. Soils in Massachusetts 1-49
7. Rare Plants on Rights-Of-Way 1-53
APPENDIX II: INFORMATION ON INDIVIDUAL HERBICIDES.
II-l
A. AMINOTRIAZOLE
B. AMMATE®
C. ATRAZINE .
D. BROMACIL .
E. 2,4-D . . .
F. DICAMBA . .
G. DIQUAT . .
H. DIURON . .
I. GLYPHOSATE
J. KRENITE®
K. METOLACHLOR
L. PICLORAM .
M. TEBUTHIURON
N. TRICLOPYR .
II-3
11-15
11-19
11-35
11-44
11-86
11-103
11-116
11-124
11-136
11-143
11-151
11-172
11-177
BIBLIOGRAPHY
B-1
-IV-
LIST OF TABLES
Page
1. Estimated Herbicide Usage in Massachusetts .... 4
2. Comparison of Herbicide Usage by Type
of Right-of-Way 6
3. Herbicides Used on Massachusetts Department
of Public Works Highways 7
4. Mutagenicity Tests 19
5. Potential Exposure to Herbicides From
Rights-of-Way Application 24 p
6. Number of Times Common Species or Signs Were
Observed on Areas Treated with 2,4-D and 2,4,5-T . . 51
7. Limitations Imposed by Weather, Season and
Various Terrains 73 J<
8. Cost Estimates 102
9. Herbicide Cost per Acre by Type of Application. . . . 105
10. Costs per Acre of Various Treatments 106
I-l Species Implicated in Inhibition of Tree
Establishment 1-39
1-2 Rare Plants Likely to be Found on Rights-of-Way
in Massachusetts 1-51
II-l Mutagenicity Tests: Aminotriazole II-7
II-2 Indicators of Potential Ground Water
Contamination: Aminotriazole 11-12
II-3 Toxicity of Aminotriazole to Birds 11-13
II-4 Indicators of Potential Ground Water
®
Contamination : Ammate 11-17
II-5 Acute Oral Toxicity of Atrazine 11-20
II-6 Mutagenicity Tests: Atrazine 11-23
II-7 Indicators of Potential Ground Water
Contamination: Atrazine 11-30
II-8 Toxicity of Atrazine to Fish 11-32
II-9 Toxicity of Atrazine to Lower Aquatic Organisms . . . 11-34
11-10 Mutagenicity Tests: Bromacil 11-38
11-11 Indicators of Potential Ground Water
Contamination: Bromacil 11-43
11-12 Variations in SolubiHty of 2,4-D 11-45
11-13 Acute Toxicity of 2,4-D 11-46
11-14 Mutagenicity Tests: 2,4-D 11-56
-V-
11-15 Persistence of 2,4-D in Soil 11-64
11-16 Degradation of 2,4-D by Microorganisms 11-67
11-17 Residues of 2,4-D in Water 11-68
11-18 Indicators of Potential Ground Water
Contamination: 2,4-D 11-72
n-19 Toxicity of 2,4-D to Birds 11-74
11-20 Toxicity of 2,4-D to Fish 11-76
11-21 Toxicity of 2,4-D to Lower Aquatic Organisms .... 11-79
11-22 Toxicity of 2,4-D to Livestock 11-82
11-23 Acute Oral Toxicity of Dicamba 11-87
11-24 Mutagenicity Tests: Dicamba 11-92
11-25 Indicators of Potential Ground Water
Contamination: Dicamba 11-97
11-26 The Effect of Dicamba on Birds 11-98
11-27 The Effect of Dicamba on Fish 11-100
n-28 The Effect of Dicamba on Lower Aqautic Organisms . . 11-101
11-29 Mutagenicity Tests: Diquat 11-106
11-30 Indicators of Potential Ground Water
Contamination: Diquat 11-111
11-31 Toxicity of Diquat to Fish 11-113
11-32. Toxicity of Diquat to Aquatic Invertebrates .... 11-114
11-33 Mutagenicity Tests: Diuron 11-119
11-34 Indicators of Potential Ground Water
Contamination: Diuron 11-122
11-35 Mutagenicity Tests: Glyphosate 11-126
11-36 Indicators of Potential Ground Water
Contamination: Glyphosate 11-129
11-37 Toxicity of Glyphosate to Fish 11-130
11-38 Effects of Temperatures on Toxicity of
Glyphosate to Fish 11-133
11-39 Toxicity of Glyphosate to Lower Aquatic Organisms . . 11-134
11-40 Indicators of Potential Ground Water
Contamination: Fosamine Ammonium 11-140
11-41 Indicators of Potential Ground Water
Contamination: Metolachlor 11-148
11-42 Effect of Metolachlor on the Reproductive
Success of Birds 11-149
11-43 Mutagenicity Tests: Picloram 11-157
-VI-
11-44 Indicators of Potential Ground Water
Contamination: Piclorara 11-163
11-45 Toxicity of Picloram to Birds 11-164
11-46 Toxicity of Picloram to Fish 11-167
11-47 Toxicity of Picloram to Lower Aquatic Organisms . . . 11-168
11-48 Indicators of Potential Ground Water
Contamination: Tebuthiuron .......... 11-175
11-49 Acute Oral Toxicity of Triclopyr 11-178
11-50 Indicators of Potential Ground Water
Contamination: Triclopyr 11-181
LIST OF FIGURES
1. Herbicides grouped according to mobility
and toxicity 80
II- 1 Concentrations of bromacil in soil:
6 weeks after treatment II-40A
II-2 Concentrations of bromacil in soil:
23 weeks after treatment II-40A
-vii-
ABOUT THIS REPORT
This Generic Environmental Impact Report (GEIR) examines the practice
of vegetation control on utility and railroad rights-of-way in
Massachusetts. The report focuses primarily on the use of herbicides,
but also describes other control alternatives such as manual and
mechanical control, as well as the potential for biological control on
rights-of-way.
The topics to be discussed in this report were identified by an informal
survey of interested parties, including environmental groups, railroad
and utility companies, local and state officials, and others. These
individuals and groups were asked to identify issues which they felt
should be addressed in the study. This process resulted in a broad
range of topics which have been covered in this Generic Environmental
Impact Report. Since the report had to be completed in four months,
however, not all the topics could be addressed in equal detail. Most of
the available resources were allocated to the development of a scientific
base of information regarding the toxicity and mobility of fourteen
herbicides used in Massachusetts for vegetation control on
rights-of-way .
The report is divided into three sections:
1. The main body presents an overall discussion of the major
topics of this report such as alternative control measures and
descriptions of vegetation control problems.
2. Appendix I presents supplemental information on a variety of
topics .
3. Appendix II presents a literature review on the fourteen
herbicides. For each herbicide in Appendix II, the following
information is presented:
- Acute and subacute /sub chronic toxicity by oral, dermal, and
intraperitoneal administration (where data are available), as
well as information on eye and skin irritation;
Special toxicological studies, including carcinogenicity,
teratogenicity, and mutagenicity;
-1-
- Fate in soil and water, including leaching potential,
dissipation times, run-off potential, and degradation rates;
and
- Effects on non-target organisms, including birds, fish, lower
aquatic organisms, bees, and other organisms.
Summary statements about the literature are included in the main body
of the report. These summaries are purposely brief so that the reader
will not be tempted to rely on them, but rather on the full complement
of information in Appendix II. Accompanying the summary statements
in the main body of the report are general discussions which interpret
the data presented in Appendix II. These discussions also present
site-specific factors that must be incorporated into an analysis of
impact.
Secondary source material (i.e., reviews of original studies) was used
whenever possible because of the limited time available for the
preparation of this report. Secondary source material was found to be
adequate in assessing the acute toxicity of the herbicides, as well as
their impact on non-target organisms. However, this material was
found to be uneven in its coverage of important topics concerning the
mobility and persistence of the herbicides; primary sources (original
studies) were obtained to supplement where necessary. In regard to
chronic toxicity, the secondary source material was considered
inadequate and primary sources were used in most instances. Primary
and secondary sources are identified in the bibliography at the end of
this report.
-2-
^
OVERVIEW
Public concern is growing about the introduction of chemicals into our
environment. Lately, herbicides have been given particular attention
because of the controversy regarding the use of Agent Orange in
Vietnam. (Agent Orange, named for the color of the storage drums, is
a 50:50 mix of butyl esters of 2,4-D and 2,4,5-T and contains a type of
dioxin that is known to cause serious health effects.) In
Massachusetts, railroad and utility rights-of-way have become the focus ^
of concern about herbicides despite the fact that herbicides are used "^
for many other purposes. Before presenting information regarding
vegetation control on rights-of-way, it is important to understand the
overall picture of herbicides usage in Massachusetts and the significance
of their use on rights-of-way. v
I
In Massachusetts, herbicides are used in agriculture, on residential
lawns and gardens, on parks and recreational land, golf courses, and
on commercial grounds. For each of these uses. Table 1 shows the
estimated acreage treated with herbicides, the total amounts of
herbicides used (as pounds of active ingredient) , as well as major
herbicides in each market. This information was generated from f
interviews with distributors, large scale sellers of herbicides, lawn
service firms, members of the Cooperative Extension Service, and other
members of the technical support community. Because of the lack of a
reliable data base regarding the quantities of herbicides used in
Massachusetts, most estimates are presented as ranges of values.
Agriculture represents the biggest use of herbicides in Massachusetts,
with an estimated 161,000 to 320,000 lbs of herbicide used on 193,000
acres (rate of usage = 0.83 to 1.66 lbs /acre). Within agriculture, the
production of field corn and cranberries uses the greatest amount of
herbicide. Another major use of herbicides is on residential lawns,
where 55,000 to 110,000 lbs of herbicides, usually "home and garden"
formulations, are applied to a total of 160,000 to 210,000 acres (rate of j
usage = 0.26 to 0.69 lbs/acre). Lastly, herbicides are used on
{
-3-
<
H
H
W
O
<
<
2
w
u
Pi
O
u
w
H
W <
a u
<
W
P
I— t
o
I— (
Pi
Q
W
H
O
W
Q
w
<
I— I
H
(U
»4
u
'0
0
0
2
1— •
'3
^4
• r4
u
u
JC
.'0
o
'3
o
(U
«> u
«» t.
13
lobenil,
opmami
X
ne,
chlo
ne,
chlo
0
..1 3
•5^
N 1—1
U
Q ^
-0 TD
rt 0
OJ 0
H
•^ S
E
1 ^
nJ 0
^ tt
^ t1
O D-
rr C
0) U
•«-> <u
•M <U
•r «*
- <u
J O.
< B
< E
W
Q C
z
CO ,D
<
<
<
04
0U
111
o
u
O
Q
Q
Q
«k
*
*
Qp:
oo:
9 a:
4^0.
^ Pu
4a.
*u
*U
-O
^2
(M 2
(Nl 2
•k
«k
«k
«5 cT
-Q .2
-^ .2
E ^
E "Tx
£ "r.
rt 2^
rt ^
^ 2i
o c
o fi
o C
.P- (U
.^ (U
.PH 0)
Q^
Qi2
Q J3
X
o
o
o
*
o
CM
CO
I
o
o
o
o
o
o
o
o
o
o
o
«k
o
o
o
o
«
o
CO
I
o
o
o
o
o
o
•k
o
I
o
o
o
o
o
o
«k
o
00
I
o
o
o
«k
o
o
o
o
o
o
o
«
*
o
o
CO
1
o
o
1
o
o
o
o
o
•k
1— (
ID
in
o
o
o
o
o
o
? s
I
o
o
o
■k
sO
I
o
o
o
«k
sO
CO
o
o
o
•k
o
CO
I
o
o
o
00
o
o
o
«k
o
CO
I
o
o
o
I.
(
«
I
«
c
R
O X
o «
o
o
*
o
o
o
o
>£»
I
o
o
CM
in
CO
(U
<u
o
<
(U
■»->
£
en
w
o
o
o
o
o
o
O
o
o
o
o
o^
o
o
o
o
o
o
o
o
o
o
o
(M
o
o
in
in
o
o
o
o
o
o
o
r-
«k
•k
*
«h
•k
•k
i^
«k
«k
*
•k
*
CO
in
c^
CO
(VJ
in
o
p-
fN3
in
o
"^
o^
^
f-i
CM
i-H
<M
rr
CO
in
1— 1
r-H
r— 1
r^3
1
o
o
o
•k
o
1
o
o
o
*
o
o
1
o
o
o
•k
00
CM
1
o
o
o
O
CO
>>
u
c
(A
o
(U
>H
0
;h
ao
;.
o
o
(0
;h
v
3
U
^^
0)
<u
•«->
•♦-»
o
Xi
U
:3
T3
l-H
(U
c
•1^
^
o
$M
(U
CO
fa
w
0.
U
P
<
o
u
u
o w
^ >
u
o
c
O E
(0
C
J
-t->
13
en
0)
Pi
c
o
(n
C
t3
C
a- <^
^ 2
*
en
C
o
u
;h o3
tn
a.
i:
?
41
0
9
c
«
•c
h
l«
tK
en
a>
4)
(U
en
•D
en
p
S
en
3
4)
T)
c
(0
>N
(U
•f"
h
nJ
•«-»
3
0
U
u
1
u
0)
l-H
^
c
E
0
w
a
1— H
E
1
■4->
p^
0
o
^
nS
^
a
O
•i-i
eri
O
H
i
i
municipal and institutional land holdings, primarily on golf courses and
commercial grounds. A total of 36,000 to 70,000 lbs of herbicides are
applied in this category to an estimated area of 100,000-127,000 acres
(rate of usage = 0,28 to 0.70 lbs /acre).
The use of herbicides on rights-of-way contributes roughly 17%-29% of
the total use of herbicides in Massachusetts, with an estimated 100,600
lbs applied in 1981 to 14,729 acres (rate of usage = 6.83 lbs/acre).
Within the rights-of-way category, the contributions from railroad,
utility, and highway rights-of-way are shown in Table 2. Railroads use ^
the most herbicides in terms of pounds of active ingredient (49,100 lbs
used by railroads in 1981 as compared to 35,000 lbs and 32,400 lbs for
utilities and highways, respectively. The rate of use is highest on r
railroad yard and line maintenance (12.8 lbs /acre) and lowest on rail-
road brushwork (3.5 lbs / acre) .
All data, except that provided by one utility company, are for 1981.
That year was considered to be more representative than recent years
because of the supension of treatment in certcdn areas pending reso-
lution of regulatory questions (see Appendix I, Chapter I).
This report focuses on rcdlroad and utility rights-of-way, since the use
of herbicides on highways has decreased considerably in the last few
years due to budget constraints. Information from the Massachusetts
Public Works Department indicates that herbicide use (in pounds of
active ingredient) decreased by about 40% from 1981 to 1982. At the
same time, the percentage of roadway treated with herbicide decreased
from about 4.2% to about 1.8%. (The rate of usage, however, increased
from 5.96 to 8.39 lbs /acre.) The purpose of vegetation control on
highways is to aid in snow removal, reduce snow drift, reduce mainte-
nance costs in ditches and shoulders (including the need to keep guard-
rails clear), control poison ivy, and increase the safety of motorists.
Table 3 shows the herbicides used for state highway maintenance in
1981 and 1982. In both of those years, about 6400 acres were main-
tained by mowing. Additional information about the vegetation control
on highways is provided later in this report (see Information Requested
by Reviewers) .
-5-
I
<
<
Q
00
•
l-H
(A
(TJ
(fl
■4J
c4
o
2
o
C
■*-»
•^
c
(U
o
(0
P
p
0)
T3
•1^
C
Xi
o
u
O
(U
pC
i-H
I
00
OP
o
I-H
I
I
CO
<
O
H
X
a
u
n)
CO
^ -^
u (U
bran
in lin
u
0
-73 B
iD
CD
CO
CO
00
^ ^
•
3
c
>o
c
rt ^3
CO
h
-^
o^
sO
>> C
^
e
-^ rt
■^-^
ir>
W
<
CX4
o
>^
H
>^
P3
O
cn
P
Q
I-H
u
HH
PQ
X
O
z
o
w
I-H
<
o
u
CO
T3
lU
(U
u
•4->
o
rt
<
H
Vj CO
o
0 (U
o
- '0
rH
CO .i;
•t
tj o
o^
^
O a;
CU X
in
00
CO
>^
Rt
^
1
^^^
P
1
^
bfi
•IH
PS
MH
-d
0
<d
0
<u
^4
a
1— t
>>
(3
H
p(i
o
■^
o^
(M
o
CM
I-H
r-
C^
00
fva
aw
o
o
o
o
o
o
o
in
•sO
0)
«h
*
«
c
in
vO
o
•S
CO
I-H
o
^-^
r— 1
a
<
MH
0
CO
CJ
o
I-H
CO
>s
-0
nj
3
>^
^
I— 1
•<->
r-*
CJ
I-H
• IH
^
&0
a
+*
C
t-H
•*-»
•i-i
o
D
EC
H
*
i
TABLE 3
HERBICIDES USED ON MASSACHUSETTS DEPARTMENT OF
PUBLIC WORKS HIGHWAYS
1981
1982
Herbicide
Amount
Acreage
Amount
Acreage
Karmex (diuron)
5425 lb
207
4694
lb
180
Aminotriazole
6905 lb
1584
1717
lb
394
Fenavar
(aminotriazole,
bromacil, and
fenac)
286 lb
384
231
lb
310
®
Dowpon M
(dalapon)
3207 lb
127
2789
lb
110
Krenite
399 lb
388
103
lb
100
Weedone 170®
(2,4-D and
2,4-DP)
118 lb
41
147
lb
51
Spike®
(tebuthiuron)
95 lb
25
10
lb
3
1
Fenavar
41 lb
8
80
lb
16
Total acres
2764
1164
Total Acreage = 65,000 (approximate).
Historical Practices on Railroad and Utility Rights-of-Way
The most significant event in the history of vegetation control on
rights-of-way has been the development of herbicides. Although
herbicides had been around since 1850, they did not become commonly
used until the mid-1940' s when 2,4-D was discovered, initially as a
plant growth stimulant and then as an herbicide. In 1948, another
phenoxy compound, 2,4,5-T, was introduced and immediately found
extensive use along rights-of-way because it was more effective against
-7-
woody plants than 2,4-D. After these two chemicals came onto the
market, a large number of additional herbicides were developed. By
1950 there were 15 herbicide active ingredients on the market. By 1980
there were 180 herbicide active ingredients available in 6000
formulations .
On railroad rights-of-way, a variety of methods were used before the
introduction of herbicides in the 1940' s. These included
application of waste oil to the ballast area
- heavy applications of salt
controlled burns 3 to 4 times a year
- applications of arsenical compounds
After 1950, however, herbicides quickly became the primary means of
control in railroad yards, and on branch and main lines. In
Massachusetts, brush control along the sides of the railroad continued
to be done manually until the early 1970' s, when herbicides became the
preferred alternative.
On utility rights-of-way, vegetation was controlled manually before the
1940' s. Undesirable vegetation was cut with axes and brush-axes on an
average of every three years. The workers who performed the cutting
came from Quebec, Canada, and lived on the rights-of-way in tents or
trailers during the cutting season. Chainsaws and brush-saws began to
be used on the rights-of-way in the late 1940' s. At the same time that
herbicides were introduced, the availability of the Canadian woodcutters
decreased as the economy of Quebec improved and immigration laws
became stricter. The conversion from cutting to herbicide control
began around 1955, at which time spraying was done mostly by
hydraulic sprayers mounted on four-wheel-drive trucks or all-terrain
tractors. Helicopters were used in some areas of difficult terrain in the
western part of Massachusetts. In the early 1960's selective basal and
foliar treatments (explained below) began to be the primary treatment
methods. Helicopters were last utilized in 1971.
-8-
Vegetation Control Problems on Rights-of-Way
Utility and railroad rights-of-way present considerably different
vegetation control problems, and different approaches are used to solve
those problems. On utility rights-of-way, only a subset of the
vegetation needs to be removed, namely trees and woody growth around
structures. Trees must be removed because they can fall into lines or
cause "flashovers" or "arcing" between the trees and the line, causing
breakage or short circuits. The allowable potential heights of trees
varies according to the heights of conductors, allowing for sag under
ice-laden conditions. Allowable heights are 10 feet for 345 kV lines, 8
feet for 115 kV lines, and 20 feet for side strips (where tree falls could
cause a problem) . Vegetation control on utility rights-of-way is
therefore selective, attempting to eliminate .trees whose potential height
is above acceptable levels, and preserving vegetation whose potential
height is below this level. Around structures and on access roads,
target vegetation includes all woody vegetation that may hinder routine
inspection and maintenance of the line. In these areas, non-target
growth is limited to herbaceous species.
A different situation exists on railroad rights-of-way where the goal is
to eliminate all vegetation in train yards and on branch lines and main
lines. If allowed to become established on the right-of-way, vegetation
could increase the amount of organic matter under and around the
track, resulting in water retention, drainage problems, and an
increased rate of decay of wooden ties. The requirement to maintain a
vegetation- free area, or even to severely restrict vegetation, demands a
different approach to vegetation control than that practiced on utility
rights-of-way. There is no possibility of selectively treating desirable
and undesirable vegetation. A number of different active ingredients
are generally used in combination so that the maximum number of target
species can be eliminated. (On utility rights-of-way, applications
involve usually only one, sometimes two, active ingredients). The
mixtures of different herbicides are applied evenly over the lines and
yards, rather than applied on certain plants.
-9-
"Brushwork" on railroad rights-of-way, on the other hand, is similar in
many ways to the control of vegetation on utility rights-of-way.
Brushwork involves the control of woody vegetation adjacent to the
ballast. The width of the brush control area depends on the location
and height of potentially dangerous trees, but is commonly 20 to 25
feet. The purpose of this activity is to maintain visibility and prevent
the disruption of communication lines. Brushwork involves the selective
treatment of tall-growing and the encouragement of desirable low-
growing shrubs and herbaceous growth.
i
-10-
THE HERBICIDE ALTERNATIVE
The following section discusses the use of herbicides on railroad and
utility rights-of-way. It describes current practices, and then
introduces the individual chemicals that are commonly used. Most of
this section is devoted to a discussion of the toxicity and mobility of
these herbicides and ways to minimize their impact.
CURRENT PRACTICES
Railroad Rights-of-Way
Herbicides are applied to lines and yards by means of a high-rail
vehicle which can move both on and off the track. The vehicle moves
10 to 15 miles per hour and sprays herbicides from lateral arms located
12-18 inches off the ground. The nozzles are spaced 20-24 inches
apart and have typical flow rates of 2-3 gallons /minute at 40 pounds
per square inch pressure. Both pre-emergent and post-emergent
herbicides are used. Pre-emergent herbicides, such as metolachlor, are
ones that are applied before the weeds emerge. On rights-of-way in
Massachusetts they are applied in April and early May. Post-emergent
herbicides, such as 2,4-D, are ones that are applied after the weeds
emerge. On rights-of-way in Massachusetts post-emergent herbicides
are applied in June and July. Different types of lines (e.g., main
lines vs. branch lines, branch lines with and without ballast, etc.)
receive different treatments, either pre- or post- emergent, or both.
Since it prevents any vegetation from emerging, pre-emergent treatment
is used where control of vegetation is particularly important — in yards
where slippage would endanger yard workers, for example.
®
Typical herbicides used on railroad yards are Atratol (atrazine) , and
®
Karmex (diuron) . Branch lines may be treated with these herbicides
or with 2,4-D, diquat, ametryn, or Banvel 720 (a combination of
dicamba and 2,4-D). Usually three or four of these products are mixed
together and applied with a water solvent. The total amount of applied
-11-
material is on the order of 40 gallons /acre; the number of pounds of
active ingredient per acre varies with the particular combination of
products used. (A double track 35 feet wide equals roughly 4.25
acres/mile). Applications in yards and on branch and main lines are
made every year.
In brushwork, the high-rail vehicle is equipped with nozzles (at the
end of lateral arms) designed to limit the drift of the material to the
edge of the right-of-way. In Massachusetts, a typical mixture used in
brush control is Roundup (glyphosate) combined with Garlon 3 A
(triclopyr) mixed with water. Twenty-five gallons of mixed material is
used per acre.
Utility Rights-of-Way
Herbicides are applied to utility rights-of-way by a variety of
application techniques :
Basal spraying is the application of herbicide, usually in an oil carrier,
to the root collar, exposed roots, and the lower 18 inches of the trunk.
The material is released as a directed spray of a large droplet size.
Basal spraying can be done year round (except in deep snow) by
backpack or hydraulic sprayer.
Foliar spraying is the application of herbicide, usually in a water
carrier, to the leaf surfaces of the entire plant. In order to assure
maximum coverage the material is often released in a "mist" of small
droplet size. Larger droplet sizes are also effective, however, and
thickeners that increase the droplet size are often added. Surfactants
may also be added since they increase the spread of the material on
the leaf surface. Foliar applications are limited to summer months,
along with late spring and early fall, and can be done with a backpack
or hydraulic unit.
Cut stump treatment is the application of the herbicide to the cut
surface of a stump, and sometimes the root collar and exposed roots.
In Massachusetts, a sponge applicator has been developed which
-12-
effectively controls the amount of herbicide released. Stump treatments
are not feasible when there is deep snow cover or when there is sig-
nificant sap flow from the stump in late winter/early spring.
Dormant stem spraying is the application of the herbicide to all exposed
wood when the foliage is absent from the plant. The root collar and all
stems are thoroughly drenched. An oil carrier is used to increase bark
penetration.
Dry herbicide application involves the application of herbicide in the
form of pellets, granules, or beads to the soil surface near undesirable
species. Rainfall moves the herbicide through the soil where it can be
taken .up by plant roots.
Other techniques not commonly used in Massachusetts include frilling ,
in which dry herbicides are placed in shallow V-shaped cuts in the
bark, and tree injection, in which herbicide material is injected into the
cambium layer with a device that wounds the tree and inserts the
herbicide in one operation.
The herbicides used on utility rights-of-way differ considerably among
utilities. In 1981, for instance. New England Power Company and
®
Massachusetts Electric Company used primarily Krenite , as well as
mixtures of picloram and 2,4-D (Tordon 101 , Tordon RTU ), along
with a mixture of Tordon 101 and Garlon 3A (triclopyr) . Northeast
®
Utilities, on the other hand, used Ammate XNI (ammonium sulfamate) ,
(S) (S)
in water, Krenite (fosamine ammonium) in water, Garlon 4 (triclopyr)
®
in kerosene, and Banvel CST (dicamba) without dilution as a stump
treatment.
HERBICIDES COVERED IN THIS REPORT
After consultation with applicators, utilities, and railroad companies,
fourteen herbicides were found to be important in the control of
vegetation on rights-of-way in Massachusetts. The following information
briefly introduces these herbicides.
-13-
Aminotriazole is a post-emergent, non-selective herbicide mixed with
water that slowly inhibits chlorophyll formation over two to three
weeks.
®
Ammate is a post-emergent herbicide mixed with water that kills plants
on contact or after translocation within the plant.
Atrazine is a selective, pre-emergent and early post-emergent herbicide
mixed with water that inhibits photosynthesis,
Bromacil is a pre- and post-emergent herbicide mixed with water that
inhibits photosynthesis .
2,4-D is a post-emergent, selective herbicide usually mixed with water,
although oil-soluble formulations and granules are sold. This herbicide
kills plants by causing them to grow too quickly.
Dicamba is a pre- and post-emergent, selective herbicide mixed with
water or used as granules. It kills plants as they germinate by
interfering with protein synthesis.
Diquat is a post-emergent, selective herbicide mixed with water that
inhibits photosynthesis and also acts as a plant dessicant.
Duiron is a pre- and post-emergent non-selective herbicide mixed with
water that inhibits photosynthesis.
Glyphosate is a post-emergent, broad-spectrum herbicide mixed in water
that blocks cell metabolism by inhibiting synthesis of aromatic amino
acids.
®
Krenite is a post-emergent growth regulator mixed with water which
inhibits the normal development of leaf buds.
Metolachlor is a pre-emergent selective herbicide mixed with water that
inhibits the growth of seedlings.
-14-
Picloram is a post-emergent, selective herbicide that can be used
®
undiluted, as pellets, or, when combined with 2,4-D as Tordon 101 ,
mixed with water. The herbicide disrupts the formation of a number of
plant tissues.
Tebuthiuron is a pre-emergent, non-selective herbicide, applied dry or
as pellets, which must later be washed into the soil by rain and taken
up by the roots.
Triclopyr is a post-emergent, selective herbicide mixed with water that
disrupts the formation of a number of plant tissues.
EFFECTS OF HERBICIDES ON PUBLIC HEALTH
The potential hazard to humans from the use of herbicides on
rights-of-way is a function of (1) the amount of harm the herbicide
causes in the body (toxicity), and (2) the amount of herbicide that
reaches the body (exposure) . The first part of this section describes
the potential toxic effects of the herbicides and the types of toxicity
tests discussed for each herbicide in Appendix II. The second section
is a general discussion of the potential routes by which humans may be
exposed to herbicides used on rights-of-way. Finally, this section
summarizes the information presented in Appendix II regarding the
toxicity of the individual herbicides.
Toxicity
The term toxicity refers to any deleterious effect produced by a
chemical or physical agent on a biological system. Toxicological data
can be divided into four general categories: acute, subchronic,
chronic, and special studies. Since special studies are often the most
critical and controversial, this discussion begins with an overview of
carcinogenicity, mutagenicity, and teratogenicity.
Carcinogenicity Cancer is characterized by the unrestrained growth of
daughter cells from an original target cell. This target cell is assumed
-15-
to have been modified by one or more events in which the DNA and/or
other cellular regulatory mechanisms were altered. Details of the
cellular and biochemical events leading to tumor formation and
progression to malignancy are not clearly understood. The growth and
spread of cancer has been shown to depend in part on host factors
such as hormonal and immunological status and genetic background, as
well as a variety of modifying factors such as lifestyle (diet, tobacco
use, alcohol, stress).
Three major types of information can be used to identify agents that
may pose a carcinogenic hazard to humans. They are:
epidemiologic evidence derived from studies of exposed human
populations ;
- experimental data from long-term tests in animals, and
- supportive evidence derived from short-term tests whose results
correlate well with in vivo carcinogenic activity.
Human data provide the most secure basis for evaluating the
carcinogenic effects of an agent. However, in regard to the herbicides
covered in this report, epidemiologic studies are limited by imprecise
data on exposure. A major source of this imprecision is the long and
variable latency period (ranging for 2 to 40 years) between initial
human exposure and clinical manifestations of cancer. Another
drawback is the necessarily limited size and availability of test
populations.
In the absence of suitable human data, animal tests (with their
associated extrapolation uncertainties) are utilized to provide the best
information available to assess carcinogenic risk to humans. Typically,
both sexes of a species (usually a rat or a mouse) are used; the test
substance is administered continually by the selected route of
administration from weaning through the major portion of the animal's
life or until death. The amounts of material administered are often the
maximally tolerated dose and half that amount.
-16-
Evidence of carcinogenic activity for the herbicide or other test
substance can be demonstrated in one of three ways:
1. By induction of a tumor type not usually observed in the test
species;
2. By induction of an increased number of a tumor type normally
seen; or
3. By the appearance of tumors at a time earlier than would
otherwise be expected.
The uncertainties in employing animal tests to determine the
carcinogenic hazard to humans are numerous. Some of the more
important factors are species differences, genetic variability, metabolic
capabilities, body weight, lifespan, and DNA repair capabilities. Animal
studies are also often performed at high doses to ensure that a
statistically significant incidence of tumors is produced in the relatively
small population of test animals usually used in such tests. These
results must be extrapolated to much lower exposure levels typical of
human situations.
Short-term tests, which measure the induction of neoplastic cell
transformation in cultured mammalian cells, can provide useful
supportive information. (Neoplastic growth is new tissue growth that
serves no physiologic function.) These tests are rapid, less costly,
and require significantly less sample than whole animal testing. On the
other hand, they are imprecise because they do not completely mimic
whole body reactions. Transformation assays involve the treatment of
cultured mammalian cells with materials to see if they convert the cells
to a pattern of unrestricted growth. Results accumulated to date show
a good correlation between transformation response in cell culture and
carginogenicity in whole animal studies. The major disadvantage of
these tests is the lack of reliable metabolic activation systems. This
factor is important because many known carcinogens exert their
influence in humans and experimental animals after metabolic conversion
in the body to the active form.
Mutagenicity A mutation can be defined as any heritable change in the
genetic material of a cell or organism. The health consequences of
-17-
deleterious mutation in human populations is poorly understood. It is
commonly believed, however, that mutations are invariably harmful to
human health. Among the possible sequelae of a mutation are cell
death, altered structure and/or function, or no overt immediate effect
(should the mutation be unexpressed by virtue of its recessive nature).
An agent constitutes a genetic risk to future generations only if its
mutagenic potential is realized in germ cells (i.e., eggs or sperm).
Somatic (non-germ cell) effects are also important in that they may lead
to cancer, terata, or aging phenomena in an individual, but the risk to
society is less since that effect is not transmitted to future generations.
The current consensus among geneticists is that four test systems
provide the highest degree of confidence in assessing mutagenicity.
These are the mouse heritable translocation test, the mouse
specific-locus test, the rodent dominant-lethal test, and the mouse in
vivo somatic mutation test or spot test. Many of the herbicides covered
in this report have been examined in these test systems. Positive
results in these tests are reliable indicators that the mutagen has
reached the germ cells and affected their genetic constitution in a
manner that can be detected in resulting progeny.
Positive findings in one or more of the remaining battery of
non-heritable genetic tests may be indicative of the possibility of
heritable effects, but they do not constitute definitive evidence that a
substance poses a hazard to humans. For instance, the significance of
positive findings in in vitro cytogenetic tests is questionable due to the
lack of repair mechanisms, metabolic processes, etc. that would be
present in a whole animal system. Results in bacterial systems are
even further removed from the human exposure scenario. Differences
in the organization of DNA in prokaryotic (bacteria and blue-green
algae) and eukaryotic (animals) organisms make it necessary to test for
mutagenic capability in both systems.
Table 4 contains a list of mutagenicity tests currently in use. They
are in rough order of decreasing value with respect to predicting
results for germ cell mutagenesis in vivo. The list is by no means all
inclusive, but includes most of the tests reviewed in Appendix II.
-18-
TABLE 4
MUTAGENICITY TESTS (IN ORDER OF DECREASING VALUE)
Test System
Mouse Heritable Translocation
Mouse Specific-Locus
Mouse Dominant Lethal
Mouse In Vivo Somatic Mutation
(spot test)
Comments
Directly measures inherited chromo-
somal damage in a mammal. Detects
reciprocal translocations (the shift
of a portion of a chromosome to
another part of the same
chromosome or to another chromo-
some). These reciprocal
translocations are of concern be-
cause offspring of carriers have a
high probability of inheriting
aneuploid genomes that can result
in death and /or major defects,
(aneuploid = an organism whose
somatic nuclei do not contain an
exact multiple of the number of
chromosomes) . Mutant F^ animals
are detected by deviations from
normal fertility or by cytologically
detected chromosome aberrations.
The only established test that
directly measures inherited point
mutations (affecting only one or a
few DNA base pairs in a gene) in a
mammal. Mutant F- animals are
generally scored on the basis of
phenotype (i.e., a detectable
expression of a mutation) .
Scores all genetic events that cause
the deaths of offspring as early or
mid-term embryos. Since mutants
are dead they cannot be genetically
tested, but this test is a signal
that other types of chromosomal
damage are also being induced.
Detects expression of recessive coat
-color genes for melanocyte
precursor cell of a midgestation
embryo. The test is significant
-19-
In Vivo Mammalian Cytogenetic
because it is an in vivo mammalian
test capable of detecting both gene
mutations and various kinds of
chromosomal damage and because it
provides evidence that heritable
genetic alterations may be induced.
Measures chromosomal aberrations
(structured or numerical) . The
majority of spontaneous abortions in
humans are associated with
chromosomal aberrations.
Sister-Chromatid Exchange
A reciprocal exchange of segments
between sister chromatids of a
chromosome. Significance to hu-
mans is not known.
In Vitro Mammalian Cytogenetic
Measures chromosomal aberrations
induced in culture.
Drosophila Sex-linked Recessive
Lethal
Detects mutations on X chromosome
('V'20% of entire genome).
Yeast Mitotic Recombination
Detects genetic damage brought
about by agents interfering with
the function of the spindle-fibre
apparatus. The target molecules
are specific proteins rather than
DNA.
Bacterial Reverse Mutation, and
DNA Repair
These tests such as the bacterial
Ames / Salmonella test and the E^ coli
reversion test, detect various
change in prokaryotic chromosomal
material.
-20-
Teratogenicity Another category of tests which are critical to the
assessment of hazard is teratology. Teratology is broadly defined as
the study of malformations of the newborn that occur as a result of an
adverse effect on the developing fetus. The detailed biological
mechanisms of teratogenesis are not well understood. Such factors as
nutritional status, age of the mother, placental variations, metabolic
differences, dose, and route and time of gestation at which a fetus is
exposed may all influence the potential teratogenicity of a chemical in a
particular species.
A number of terms are used to describe adverse effects on the
developing conceptus. "Embryotoxicity" can be defined as toxic effects
on an embryo during differentiation and organogenesis.
"Teratogenicity" is one type of embryotoxic effect that occurs during
the formation of major organs and physical structures, and results in a
malformation of one or more organs or structures. "Fetotoxicity" is an
adverse effect that occurs after major organs and structures are
formed, and results in a toxic or degenerative effect on those organs or
structures. Additionally, the severity of effect is generally considered
to be in the decreasing order of embryotoxic, teratogenic, and fetotoxic
effects. Fetotoxic effects (e.g., slow growth and low birthweight) are
often reversible. Confusion arises when minor effects on organs or
physical structures (minor teratogenic effects) are considered to be
fetotoxic because they do not affect the survival of the organism.
Tests for teratogenicity generally involve the administration of the
chemical to pregnant rats or mice during the critical days for
teratogenic effect (days 6 to 15 in rats). Test protocols should (but
sometimes do not) include a histological examination as well as an
observation of visible, easily measured signs of viability.
Egg injection studies have been used to assess the teratogenicity of a
number of herbicides discussed in Appendix II. In these tests, the
chemical is injected directly into chick eggs, and the effects are noted
on the percentage of eggs that hatch. These tests, however, have
-21-
limited relevance to human teratogenic effects because of the absence of
anatomical and physiological maternal-fetal relationship.
Other Toxicity Studies Aside from the three special study areas
discussed above, two other types of toxicity studies are also vital to
the assessment of hazard; namely, chronic and acute toxicity tests.
Chronic toxicity studies generally involve the administration of a
compound for a substantial portion of the lifetime of the test animal.
Such studies are designed to detect the lowest concentration that causes
no apparent effect. They also detect effects on survival, growth,
functional integrity of body organs, and reproductive capacity.
The next level of toxicological study is a subchronic or subacute test,
which involves administration of the test chemical on multiple occasions.
Experiments are generally conducted for 90 days with rats and mice,
and for six months to one year with dogs. These short-term
subchronic studies are typically conducted at higher exposure
concentrations than chronic studies. Pathological changes may thus be
more clear-cut because they occur more quickly with the higher doses
and because they are not obscured by other chronic changes, such as
aging.
Acute toxicity studies provide information on the effect (s) of a single
exposure. Acute toxicity is generally measured by the median lethal
dose (LD--) or median lethal concentration (LC(._); i.e., the dose or
concentration that will kill 50 percent of the test population under
stated conditions. Lethality provides a standard of comparison among
many substances whose mechanism and sites of action may be markedly
different. The LC_- value has general acceptance as an early warning
about potential adverse effects, but it is only roughly indicative, if at
all, of the effects of chronic exposure to small amounts of a chemical.
Acute toxicity studies also include tests to determine local effects of
chemicals when applied directly, e.g., to the skin and eyes. The major
types of local effects than can occur are irritation, corrosion, and
sensitization. An irritant effect is a reversible effect, while corrosion
-22-
causes visible destruction and irreversible alteration in the tissue at the
site of contact. Sensitization involves an immunologic mechanism.
Exposure
There are three primary ways in which the human body can be exposed
to chemicals: ingestion, dermal absorption, and inhalation. Tables 5
ranks the relative importance of these three routes to groups of people
on, adjacent to, or at a distance from rights-of-way. Since no
quantitative information was found on the exposure levels of herbicides
to any of these groups of people, the entries in this table are
qualitative judgments based on likely pathways of movement of the
herbicides .
Ingestion As shown in Table 5, ingestion of herbicides can occur in a
number of ways:
° Ingestion of contaminated water from nearby wells or surface
waters used for drinking water (discussed in the next section).
° Ingestion of residues on food grown adjacent to or on
rights-of-way.
° Ingestion of berries or mushrooms along the right-of-way.
Residues on berries may be a significant route of exposure, depending
on the stage of development of the fruit and the length of time after
spraying that the berries are consumed. Frank et al. (1983) measured
the residues of 2,4-D on raspberries, blueberries, and strawberries,
after a broadcast application of 0.8-6.0 kg /ha of 2,4-D on rights-of-way
and other sites. On red raspberries, residues were negligible if
spraying occurred during the flowering season. When 2,4-D was
sprayed on the immature raspberries, residues of 0.2 ppm were
ultimately found when the berries were ripe. When ripe fruit was
treated, residues of 2.6 to 31 ppm were found immediately after
treatment. Over a 2- to 5-week period these levels dropped to 0.1 and
3.3 ppm.
-23-
cfl
E
u
Q
*
*
*
(30
c
* -^
u "»
« E
o
u
in
W
<
2
O
I— (
H
<
U
I— I
J
a.
<
<
I
fa
o
I
en
H
X
o
O
Pi
fa
C/2
fa
Q
u
CQ
fa
a:
o
H
fa
en
O
cu
X
w
<
I— I
H
z
fa
H
O
0^
<1)
O
c
o
I— I
CO
(fl
(U
(U
»— 1
l-H
£
V3
E
• ft
0
nj
0
rt
$H
^^
u
r-^
M-t
O
<+H
o
>
>
*
c
o
•l-l
•♦->
en
c
o >^
^ u 2
^ C o
> o .2
*
^*^»*
^■s
en
^ <« ^
ter
mal
tact
o?
MH ^H C
^ »^ c
^ ^
oj OJ 0
rt « 0
<4H ffl
■^ T3 y
>-' T3 O
w DO
•X-
■X-
*
*
•X-
o
a
^ o 2
o c c
> o .2
*
a
v
C
^
o
en (U
E -r
o '^
end
icid
■X- a^
^i ^
<U Sh
i^ <u
^ -0 «
-'^
0 w^
^
13
'1-t
00
C
42
3
g
3
(0
0)
g
0
u
130
ni
4J
05
•1-4
>
•IH
&0
>^
a
c
(TJ
Q*
>^
^
f-H
•IH
^H
s
>
1
•b
flj
o
o
VM
*
U
o
u
CO
3
S
u
0
hers mi
ay
0
1
DO
C}0
•
en
1
M-4
do
0
0
^3
1
0
1
en
u
O
rs; ot
t-of-w
0)
0
■t->
(U
u
i2
• rH
>
• r-t
•t-*
0
0
1
4:
bO
ed hy
apply
!30
o
l-H
a
thers
Berr
Hike
righi
d
en
E
0
<^H
onnect
ater s
•♦->
<
O
ei
cc;
0
0 ^
C
O
<
fa
E
u
*
o
£
E
•1-1
O
»4
Q
W
2
h-l
H
2
O
O
in
J
<
w
2
O
I— t
H
<
U
I— (
<
<
I
O
I
en
H
DC
O
I— (
O
Pi
W
Q
o
t— (
W
o
H
W
P
w
O
Pu
X
<
I— (
H
2
H
O
04
■4->
o
o
■<->
o
•1-1
+->
<u
c
a
3
O
U
O
cH
•tH
>
■4-*
0
<3
•«-»
3
1— 1
US
r— 1
>^
u
■ 1-H
no
cd
0
o
1— t
•'-' ._
0
hfl >>
;-)
rolo
X!
T3
'0 1^
0)
•M
o
0)
C
(U o
0
c ;=;
o
C U2
■4-)
0 3
0
U P-
2
T3
3
en
(U
^
0
M
•M
c
>N
en 0
1-^
0 rJ
•F^ c
T3 O
p
C ^
/ — «
S C
>>
>>
1— H
1— 1
lost
ertai
•1-1
b u
4J
0
■♦->
J-. ^^
c
3
0) 0)
i2
'T3 xi
3
c c
•k
3 P
1—1 1— H
J2
r— 1
>
• rH
u
03 nJ
1-H
3
i3 X5
en
o
0
0 0
w
c
a
U U
0
o
X
0- Ou CU
o
(U
II II
II
II
*
* *
* *
*
o
I
in
CM
I
On blueberries, residues ranged between 0.84 and 10.7 ppm,
independent of ripeness of fruit or length of time after spraying (up to
37 days). On ripe strawberries, residues were 10.1 and 5.49 pptn in
two different sites, respectively. On the strawberries with residues of
5.49 ppm, a rapid decline in residues was observed over a 4-day period
(to 0.03 ppm). On the strawberries with residues of 10.1 ppm,
residues declined slowly to 6.9 ppm. Picloram residues were also
measured in strawberries. Ater 4 days, residues decreased from 0.23
ppm to non-detectable levels.
No data were found on the residues of herbicides that may be expected
on mushrooms in rights-of-way. It is possible that residues absorbed
by fungal filaments in the soil could be translocated to mushrooms.
Alternatively, herbicides may be absorbed by the small primordium when
it expands after a rainfall to form the recognizable mushroom. The
literature reviewed in Appendix II indicates picloram and atrazine
accumulate in fungi. However, no information was found on particular
species or residue concentrations.
As an interesting note, one mushroom (Lepomis lentinus) is commonly
found along railroad rights-of-way and is called the "trainwrecker
mushroom," having a reputation for causing derailments. This is an
edible but tough, woody mushroom that requires extensive cooking to
soften its tissue (Miller, 1972), a practice that is also likely to reduce
any herbicide residues.
Dermsd contact with the herbicide by applicators may be the most
significant route of exposure. Unfortunately, no estimates are
available. To determine the amount of exposure, estimates must be
made of the amount that reaches the skin and the amount that is
absorbed through the skin. The amount that reaches the skin depends
on
1. The amounts in the air, on leaf surfaces, on application
equipment, and on other surfaces to which the applicator comes
to contact;
-26-
2. The amount of contact the applicator has with unmixed material
during pouring, mixing, opening bags, etc;
3. The applicator's clothing, i.e., the degree of protection it
affords; and
4. The extent of the body, and which parts of the body, come into
contact with the herbicide.
Skin uptake or absorption through the skin is estimated by knowing:
1. The duration and frequency of contact with the herbicide;
2. the area, location, and integrity of the skin exposed; and
3. the physical and chemical properties of the particular herbicide.
In regard to this last factor, the most important information appears to
be the rate of diffusion of the herbicide through the stratum corneum
layer of the skin. Such rates are not known for most chemicals, but
estimates can be made by knowing the permeability coefficient of the
skin and the partition coefficient of the herbicide between skin and
water (often the octanol /water partition coefficient is used, but this
method has yet to be validated) .
Dermal contact can also be a route of exposure for other persons on the
right-of-way. Hikers, berry pickers, birders, and others will have
varying amounts of dermal exposure depending on the above factors, as
well as on the length of time since the last application. Weather
factors, particularly rainfall, will also be important, as well as the rates
of photodegradation and volatilization of the individual herbicides.
Inhalation Inhalation of herbicide droplets and vaporized molecules is
likely to be a route of exposure for applicators and, possibly, to those
adjacent to rights-of-way. One of the primary factors in the
determining the significance of inhalation exposure is the size of the
herbicide droplet and the amount of the herbicide that is in vapor form
(volitilized) . Droplet size is determined primarily by the size and the
shape of the nozzle orifice as well as by the pressure under which the
herbicide is released. Larger droplets (>500 microns) are generally
considered to be "drift safe," since they are too heavy to move through
the air. This droplet size, however, can be too large for some
-27-
herbicides to be effective. Thickeners, particulating agents, and
adjuvants decrease the number of fine droplets in a spray. Small
droplet sizes (10 microns and less) are particularly important because of
the ability of these particles to move through the respiratory system.
Droplets of 5-10 microns are generally deposited in the nasal passage
(where high velocities of air and changes in direction cause them to be
deposited) . Droplets of 1-5 micron size tend to settle out in the
tracheal bronchial region. Droplets of less than 1 micron, as well as
volatilized molecules, are distributed throughout the alveolar region
which represents a large and highly absorptive surface.
Herbicides can also volatilize from spray droplets or from treated soil
and vegetation, and move through the air in vapor form. Although
some volatile forms can vaporize rapidly at 65°F, most herbicide
formulations used on Massachusetts rights-of-way are low-volatile forms
and vaporize at temperatures of about 80°F or above. Inhalation of
those in drift, therefore, may be greater when application occurs
during summer periods. The volatility of a herbicide is dependent on
its surface tension, viscosity, specific gravity, cind vapor pressure
(Arthur D. Little, Inc., 1979). The vapor pressures of the 14 herbi-
cides are prescribed in Appendix II.
Summary of Toxicological Literature
The following information briefly summarizes the results of the literature
review presented in Appendix II.
Aminotriazole has low acute toxicity, but causes some effects (altered
weight gain, enlarged thyroid glands) in subchronic tests. Aminotria-
zole appears to be a carcinogen, causing tumors in both rats and mice.
It has been used as a positive control in carcinogenicity tests. Most
available studies show no mutagenic activity of aminotriazole, although
more study is needed. Insufficient data are available to assess its
potential teratogenic effect. The limited studies available show no
teratogenic effect.
-28-
Ammate has low acute and subchronic toxicity. There is insufficient
information to assess its potential as a carcinogen, teratogen, or
mutagen.
Atrazine has low acute toxicity when administered orally or dermally.
However, it appears to be an eye irritant. It appears to be non-toxic
in subchronic studies, and is rapidly eliminated. Although insufficient
information is available, atrazine does not show carcinogenic or tera-
togenic effects in available tests. It does not appear to cause repro-
ductive effects, except when administered at high doses by injection.
(Since this route of administration causes moderate toxicity in acute
tests, these reproductive effects may be a result of maternal toxicity.)
Data suggest that atrazine is mutagenic only after activation by plant
enzymes. Mammalian liver enzymes do not appear to be capable of
activation .
Bromacil appears to have low acute toxicity, although it may cause mild
skin and eye irritation. Limited data suggest that it is rapidly elim-
inated from mammalian systems. Available data do not allow conclusions
to be drawn regarding carcinogenic effect. Available teratogenic stud-
ies are negative. Bromacil does not appear to be a carcinogen or
teratogen. Some reproductive impairment was noted in one study using
bromacil in aerosol form. Bromacil does not appear to be mutagenic.
2,4-D appears to be moderately toxic in acute and subchronic tests,
and some formulations appear to be eye irritants. It is rapidly elim-
inated in mammalian systems. No clear evidence is available that indi-
cates that 2,4-D is a carcinogen, although considerable debate has been
generated on the subject and further study is needed. There is some
evidence to suggest that 2,4-D causes a weak teratogenic effect; how-
ever, the data present no firm basis for conclusion. Most reliable tests
indicate that 2,4-D is not a mutagen. Some forms of dioxin have been
found as a contamincint in 2,4-D. These forms do not include the form
of dioxin (2,3,7,8-tetrachlorodi?c|oln) , which is known to be highly
toxic. Limited information is available on the toxicity of the various
forms of dioxin that are found in 2,4-D. One of the forms, 2,7-dich-
lorodioxin, caused some increased incidence of tumors and reproductive
effects; however, the data are difficult to interpret.
-29-
Dicamba has low acute and subchronic toxicity, and is rapidly eliminated
from mammalian systems. Available tests are inadequate to assess carcino-
genicity, teratogenicity, or mutagenicity.
Diquat can be considered toxic by oral, dermal, ajid inhalation routes. No
data were found concerning the carcinogenic potential of diquat. Limited
data suggest a possible teratogenic effect. Diquat does not appear to be a
mutagen in avciilable tests.
Diuron has low acute toxicity. Slight negative effects (e.g., growth
impairment and anemia) have been observed in subchronic effects. No
tissue storage occurs, even after chronic administration. Limited data
suggest that diuron is not carcinogenic. Although there is some con-
flicting evidence, most data indicate that diuron is not teratogenic. Diu-
ron does not appear to be a mutagen, although further study is needed.
Glyphosate has low acute toxicity when administered by oral or dermal
administration. Moderate toxicity is indicated when administered intra-
peritoneally . Glyphosate appears to be readily eliminated from mammalian
systems. Although no data are publicly available, manufacturer's informa-
tion suggests that glyphosate shows no potential for carcinogenic, terato-
genic, or adverse reproductive effects. Most studies indicate that glypho-
sate is not a mutagen.
®
Krenite has low acute toxicity. A short-term eye irritation has been
observed. No data are available regarding the caircinogenic potential of
®
Krenite. Insufficient data ajre available to show with certainty that it is
not teratogenic or mutagenic. However, since Krenite® was registered
relatively recently, it can be assumed that the full complement of tests was
conducted and the results have been found to be acceptable by EPA.
Metolachlor has low acute and subchronic toxicity. Data indicate no evi-
dence of carcinogenic, teratogenic, or mutagenic effect; however, no
conclusions can be drawn based on the limited data available.
Picloram has low acute toxicity. Slight adverse effects (in organ-to-body
weight ratio) have been observed at high doses in subchronic studies.
Picloram appears to be rapidly excreted from mammalian systems. Available
data do not allow a definitive statement regarding the potential
-30-
carcinogenicity of picloram. It does, however, cause benign neoplastic
nodules, and therefore should be suspected as a possible carcinogen until
it can be shown that these nodules do not progress to carcinomas. An
insufficient amount of data are available to show conclusively that picloram
does not cause teratogenic or adverse reproductive effects. Most tests
indicate that picloram is not a mutagen, although an insufficient number of
reliable tests have been conducted.
Tebuthiuron shows moderate toxicity in acute tests. It appears to be
rapidly eliminated from mammalian systems. Although no data are avail-
able, manufacturer's information states that long-term studies have shown
no indication of carcinogenicity, mutagenicity, teratogenicity, or impairment
of reproductive performance. More publicly available information is
needed; however, since tebuthiuron was registered relatively recently, it
can be assumed that the full complement of tests has been conducted and
the results have been found to be acceptable by EPA.
®
Triclopyr has shown slight acute toxicity, while Garlon formulations have
®
low toxicity in acute studies. Garlon 3 A causes severe damage to eyes.
Although no data are available, manufacturer's information states that
triclopyr is not carcinogenic or mutagenic, but can cause adverse reproduc-
tive effects and is considered fetotoxic. More publicly available informa-
tion is needed.
POTENTIAL FOR CONTAMINATION OF SURFACE WATERS AND
GROUNDWATER BY HERBICIDES
Herbicides, like other chemicals, tend to move with the movement of water,
only more slowly. Sometimes the movement of the herbicide is so much
slower than the water that the herbicide can be considered immobile. The
movement of a herbicide in a particular area is therefore a study of (1)
the flow of water in that area and (2) the tendency of the herbicide to
move with the water, or instead, to be retained or degraded. Many of the
important parameters of herbicide mobility are a function of the particular
site under consideration. Also, parameters that are a function of the
herbicide (e.g., solubility and speciation) are highly variable among
individual herbicides. For these reasons, this discussion will avoid any
generalizations about the likelihood of particular herbicides to contaminate
surface or groundwater systems. Instead, this section wiU discuss the
-31-
possible routes of herbicide movement, focusing on the factors that
increase and decrease the likelihood of that movement. In the first
part, emphasis will be given to the site-specific factors that influence
movement. The second part of this section will identify some of the
important physical-chemical parameters of the herbicides, and will
present a summary of the literature reviewed in Appendix II,
Hydrological Considerations
When herbicides first reach the soil they can move downward into the
soil (with the infiltration of water) or they can move over the surface
with runoff water. These two pathways are competitive; i.e., the more
likely a herbicide is to move downward through the soil, the less likely
it is to move over the surface.
Subsurface Flow Much of the water that reaches the soil surface moves
downward, infiltrating through the upper soil layers. As it moves
downward it encounters first an unsaturated zone and then a saturated
one, with these zones divided by the water table. (A number of fac-
tors affect the potential for herbicides to move downward through the
soil profile and laterally at the soil surface. These factors are dis-
cussed later in more detail in regard to soil retention and mobility.)
Once the water moves through the soil into the saturated zone it is
called "recharge." Subsurface flow moves from areas of recharge to
areas of discharge. In a recharge area, the water table can be at a
considerable depth below the surface. In discharge areas, the water
table is usually at or very near the surface. For any one recharge
area, the associated discharge area can be difficult to define. This is
because recharge-discharge systems can be both localized and regional.
Local systems involve a relatively short subsurface retention time and a
nearby discharge. Regional systems involve longer retention times,
usually at deep levels, with discharge at considerable distances from
the point of entry of the water. Where there is pronounced local relief
(a hilly topography) numerous local systems of flow can be produced.
Where topographical relief is negligible, subsurface water tends to move
in regional systems. The tendency of local systems to develop rather
-32-
than regional systems also depends on the depth of the basal boundary
of the system. Deeper systems (e.g., deep unstratified glacial tills)
encourage regional flows, while shallow systems (e.g., those bounded
by unfractured granite) tend to encourage local flows.
The application of a herbicide to a particular recharge area, therefore,
can result in a very local discharge (e.g., a thousand meters away) or
introduction to a groundwater flow that extends for many miles.
Because New England topographic features can vary considerably in a
small area, herbicide applications that are only a few meters apart can
result in widely different locations of discharge.
Geologic, as well as topographic, considerations can affect the flow of
water and herbicide contaminants. Geologic control is exerted by
differences in permeability of the underlying stratigraphy. Layers with
higher and lower permeability can affect the direction and rates of flow.
A conduit with high permeability can thus move herbicides into a
regional system of ground water flow even in hilly terrain where
otherwise the movement of the herbicide would be dominated by local
groundwater flows. On the other hand, low-permeability layers can
block the expected downward flow, and move herbicides laterally to
discharge areas that are nearer the point of application than would
otherwise be expected.
Many other factors besides the topography and geology of an area
control the directions and amounts of water that move through sub-
surface systems. The infinite variety in flow systems created by these
factors (as well as the characteristics of the individual herbicides)
makes it impossible to assess the potential for groundwater contam-
ination without a site-specific investigation. As an overall general-
ization, however, local movement of groundwater may be more important
than regional movement in regard to the potential for contamination of
water supplies by herbicides applied to rights-of-way. Because of their
narrow linear form, rights-of-way are unlikely to take up a large
percentage of a regional recharge area. Dilution in a large regional
system would significantly decrease herbicide concentrations.
-33-
Additionally, since some of the herbicides have short persistence times,
the retention times of regional systems may result in degradation of the
herbicide before discharge. This is difficult to predict, however, since
conditions in groundwater systems are not likely to be as conducive to
degradation as soil conditions under which persistence times are
determined. Additional information on the persistence of individual
herbicides and the conditions for degradation in groundwater are
discussed below.
Local systems of flow may be particularly likely to occur in
Massachusetts, because of a number of conditions that may divert water
laterally away from deep regional systems:
1. Much of Massachusetts, like the rest of New England, has
pronounced local relief and therefore its groundwater is subject
to local topographic control as described above.
2. The topography of many areas in Massachusetts is bedrock
controlled, i.e., underlain by bedrock at shallow depths.
Bedrock is less permeable than most soils. Because of the
lower permeability, water may be diverted laterally at shallow
depths.
3. Bedrock can also provide high-permeability conduits for
herbicides by means of fractures in the geologic material.
These fractures can transport the herbicide in unexpected
directions, depending on the orientation and frequency of
fractures.
4. Low-permeability layers at varying depths below the surface
(called "fragipans") can divert downward movement of
herbicides to more localized lateral movement. Fragipans
consisting of compacted layers of clay are found in many parts
of southeastern Massachusetts, as well as in other parts of the
state.
-34-
Thus far, the discussion has assumed that once in the ground water
flow, herbicides will move with the movement of the water. However,
once the herbicide enters the groundwater, it can undergo a number of
reactions, including solution-precipitation reactions, changes in
speciation, oxidation -reduction reactions, ion pairing or complexation ,
adsorption-desorption reactions, and microbial degradation. A review of
the literature indicates that the last two are the most important
mechanisms for retention and degradation of the herbicides discussed in
this report. Adsorption involves the binding of herbicides by weak
chemical and physical bonds to charged surfaces of colloidal particles
(particles of less than 2 microns in diameter) along with surfaces of
silica oxides and other materials. This binding removes a certain
amount of herbicide from the solution, depending on the amount and
type of charge of the herbicide ions or molecules. More information on
this process is presented below in the discussion of adsorption of
herbicides in soil.
Microbial degradation of herbicides is probably limited in ground water
systems. Since the groundwater is not exposed to the atmosphere,
oxygen that is consumed in chemical and microbial reactions is not
replenished. Microbial oxidation of only a small amount of organic
compounds can severely deplete dissolved oxygen resulting in anaerobic
conditions. The significance of anaerobic degradation of the herbicides
covered in this report is not known. Recent studies have tried to
encourage microbial degradation of groundwater contaminants, and have
found that such degradation is significant only when nutrients and
oxygen are injected into the groundwater flow.
Surface Flow Runoff of herbicides is most likely under conditions that
encourage overland flow of water. Factors that encourage runoff
include high intensity rainfall events, long slopes with steep gradients,
low infiltration capacity of soils, and lack of vegetative cover or other
barriers to slow the movement of water. There are two ways in which
runoff can transport herbicides: (1) relatively soluble herbicides can
dissolve in water moving across the surface of soil, and (2) herbicides
-35-
that are adsorbed to soil particles can be transported during the
erosion and movement of the soil particles.
The movement of soluble herbicides in runoff is most likely to occur
when the first rainfall following a herbicide application is sufficiently-
intense to exceed the infiltration capacity of the soil. The second type
of runoff of herbicides, i.e., transport while adsorbed to soil particles,
frequently involves insoluble herbicides generally considered "immobile"
(in studies that examine the potential for downward movement). These
herbicides are often held tightly by soil particles at the surface of the
soil. During a rainfall event of sufficient intensity, these particles can
be removed and transported away from the application site. The most
important factor in determining the amount of herbicide moved in this
way is the velocity of the runoff water. Increasing the velocity by a
factor of 2 enables the water to transport particles 64 times larger
(Brady, 1974), thereby transporting a considerably larger fraction of
surface particles to which herbicides are adsorbed.
Unfortunately, many of the herbicide runoff studies determine the
amount of herbicide moved by runoff as a percentage of the amount
applied. Typical results indicate that less than 5% of the herbicide is
removed from the application area by runoff. These results lack
meaning in terms of the concentrations of herbicide contributed by
runoff to streams and other surface water bodies. Additionally, these
results can be misleading, in that low percentages lost by runoff (e.g.
"less than 1% of the herbicide") give an impression that runoff was
found to be insignificant. These small percentages can be significant
when the application involves a large portion of the drainage area of a
single stream.
Runoff water can either infiltrate into the soil (when it slows down
and /or reaches a soil whose infiltrative capacity has not been exceeded)
or it can be channeled into stream flow. Once it enters a stream, the
amount of dilution of the herbicide contamination depends on such
factors as the rate and amount of water moving in the stream, as well
as on the percentage of the drainage area that received the herbicide
-36-
application. Herbicide "sinks" in streams include plant uptake,
microbial and chemical degradation, sediment deposit, and volatilization.
If stream velocities are high, however, these sinks are not likely to be
significant, and the herbicide will move with the flow of water, either
in solution or adsorbed to suspended particles.
Once the velocity of the water decreases, as in a pond, lake, or
wetland, the sinks mentioned above become more important, and the
herbicide is more likely to be retained in the aquatic system. In
general, herbicide retention will be greatest in water bodies with
greater biomass (e.g., eutrophied ponds and wetlands) than those with
less biomass (e.g., oligotrophic lakes). Components of aquatic
ecosystems that are important in the retention and degradation of
herbicides include:
- Organic matter, both suspended and in sediments, that can
retain the herbicide by adsorption or complexation. Organic
matter can also assist in microbial degradation by providing
nutrients, and by providing carbon sources for cometabolism.
- Suspended mineral matter, which provides sites for adsorption
and microbial degradation.
Plant and animal matter, which can take up and retain
herbicides in tissue, circulating these residues from one trophic
level to the next,
- Sediments, which provide very large surface areas for
adsorption, high microbial populations, and anaerobic conditions
(which may favor the degradation of some herbicides and retard
the degradation of others).
In regard to herbicide sinks, wetlands are similar to eutrophic water
bodies in that they have a high biomass, thick sediments, and large
amounts of suspended organic and mineral matter. When flooded,
wetland soils often have a thin surface layer (i.e., a few millimeters
-37-
thick) that is an aerobic, oxidized state, overlying the remaining
sediments, which are in an anaerobic, reduced state. Wetlands that are
flooded during only a part of the year represent a particularly complex
situation for predicting herbicide retention and degradation, since the
sediments can change from an oxidized to a reduced state within a few
days after flooding.
Retention /Mobility in Soil
The upper layers of the soil provide the most significant potential for
the retention of herbicides. This is due in part to characteristics of
the soil matrix (presented below) and in part to the slower velocity of
water moving through the soil. The following soil parameters affect the
retention /mobility of herbicides:
Organic Matter Because of its large adsorptive capacity, the amount of
organic matter in the soil (expressed as a percentage of the total
volume of the soil) may be the most important determinant of the fate of
herbicides in the environment. As can be seen in Appendix II, most of
the herbicides are more mobile in soils low in organic matter (e.g., 1%) ,
and less mobile in soils with high organic content (e.g., 3%). Although
the organic matter content of Massachusetts soils varies widely, a
common occurrence is a thin (one or two inch) layer of soil with
moderately high percentages of organic matter overlying soils with
considerably lower organic content. This sharp decline in organic
matter near the surface of soils creates conditions that differ from the
conditions under which most tests of herbicide mobility are run.
Because herbicides are primarily used in agriculture, tests for mobility
often use soil that simulates agricultural conditions, i.e., soils that
have organic matter which extends deeply into the soil. Herbicide
mobility in Massachusetts soils may, therefore, be greater than
suggested by field studies available in the literature. (This would not
apply to herbicides that are easily retained by organic matter and are
applied at rates that do not exceed the adsorptive capacity of the
organic matter in the surface layer.)
-38-
Organic matter in the soil also has the ability to support microbial
popiilations responsible for degradation of herbicides. All of the
herbicides reviewed in Appendix II are degraded primarily by microbial
degradation, as opposed to chemical degradation. Generally, higher
microbial populations result in shorter persistence times. The organic
matter in the soil provides nutrients necessary for maintenance of active
microbial populations. Additionally, some herbicides are degraded by
cometabolism, i.e., degradation of the herbicides takes place only in the
presence of another carbon source, which the organic matter provides.
Soil Texture Soil is made up of particles of various sizes; the relative
proportions of particles of different sizes are generally referred to as
the soil texture. Gravels, which have a particle size range of greater
than 2 millimeters (by the International Society of Soil Science
Classification) , have a high permeability and allow rapid movement of
herbicides and other materials. Sands, which have a particle size
range of 0.02 to 2 millimeters, also have a high permeability. Because
of the high permeability, lateral movement is less likely to occur than
downward movement in both sand and gravel. Silt particles are 0.002
to 0.02 millimeters in size and have a much lower permeability, while
clays, with a particle size of less than 0,002 millimeters (2 microns)
have the lowest permeability.
Clay layers can act as fragipans, i.e., layers that slow the downward
movement of water to such an extent that they divert the water
laterally. Fragipans can be found in most parts of the state. In
southeastern Massachusetts they can be found 1 to 2 feet below the soil
surface, where they may cause seasonal flooding.
Various combinations of these particle sizes result in soil texture
classes, such as sandy clays, silty clay loams, and silt loams. "Loam"
refers to a mixture of sand, silt, and clay that exhibits overall
properties which are characteristic of the particular combination of
particle sizes. A sandy loam is a mixture of sand, silt, and clay in
which sand is slightly dominant. One of the most common soils in
Massachusetts is a fine sandy loam in which fine sand (0.02 to 0.2
-39-
millimeters) dominates. Loamy sands, which contain more sand than
sandy loams, are also common. When examining herbicide mobility
studies available in the literature, it is important to consider whether
-the soil used in the test contains as much sand as is commonly found in
Massachusetts .
Soil texture affects the lateral movement of herbicides as well as the
vertical movement. To some extent, movement in these two directions is
competitive. In a sandy loam, water can move downward about 72
inches in 24 hours and can spread to a diameter of 26 inches in the
same time period. A clay loam, on the other hand, may allow downward
movement of water to a depth of only 36 inches in 24 hours, but the
lateral spread during that time period may be 48 inches in diameter
(Brady, 1974).
Adsorptive Capacity The texture of the soil also affects the capacity of
the soil to adsorb herbicides. Particles that are less than 2 microns
(clays and some forms of organic matter) are capable of adsorbing
herbicide material by weak chemical and physical bonds. As they move
through the soil, herbicides adsorb to the charged surfaces of these
particles. Soils have varying adsorptive capacities, depending on the
amount and type of clay, the amount of organic matter, and pH. The
form of organic matter that is most likely to adsorb herbicide material is
humus — a dark, amorphous, and heterogeneous organic mass in a
colloidal state (i.e., consisting of particles that are 2 microns or less in
diameter) . Humus is what is left after microbial degradation of a
variety of organic materials. Its surface charge is generated by the
dissociation of carboxylic and phenolic groups. Herbicides may be
adsorbed onto these charged surfaces, or they may become physically
trapped in the irregular inner surfaces of the humic material.
Herbicides that are trapped in these inner surfaces are more easily
removed from the humus than the ones that are adsorbed onto the
surfaces.
Clays vary in their adsorptive capacities by the nature and organization
of their surfaces. There are three primary types, montmorrilonite ,
-40-
illite, and kaolinite, with high, medium, and low capacities to adsorb
herbicides, respectively. All three are found in Massachusetts,
although montmorrilonite is less prevalent here than in other parts of
the country. The relative adsorptive capacities of humus,
montmorrilonite, illite, and kaolinite can be expressed as a ratio of
20:10:4:1.5, respectively. One of the most important steps therefore,
in determining the ability of a particular soil to retain a herbicide is to
determine the amount of organic matter and the amounts and types of
clay that are present.
pH The acidic or basic nature of the soil solution exerts an influence
on the retention /mobility of herbicides in a number of ways. In
Massachusetts, soil pH is low, ranging from about 3.5 to 6 (see
Appendix I, Chapter 6). At a low pH, some of the adsorption sites are
not available to herbicides that enter the soil, even if the herbicides
have the appropriate charge. This is because at low pH, ions normally
present in the soil are held so tightly that they resist being displaced
by the herbicide. The adsorptive capacity of organic matter is partic-
ularly affected by pH in this way. Also, at low pH, some components
of the soil that contribute to its adsorptive capacity will change from
their usual state of being negatively charged to being positively
charged. Herbicides that are normally attracted to and held by these
surfaces will tend to stay in the solution; other herbicides, not
normally adsorbed, wiU be retained on the charged surfaces.
The pH of soil can also influence opportunities for microbial breakdown
of herbicides. Some herbicides are degraded by a variety of
microorganisms representing a wide range of tolerated pH values.
Others are degraded by specific groups of microorganisms that may
have narrower ranges of tolerated pH values. In general, fungal
degradation may be dominant at low pH values and bacterial degradation
may be dominant at pH 7 and above. Unfortunately, the role of
specific groups of microorganisms in microbial breakdown of herbicides
in the field is not well understood.
-41-
The above discussion has emphasized site specific characteristics that
determine the mobility and persistence of herbicides. Of course, the
characteristics of the herbicide itself also determine its fate in the en-
vironment. Appendix II presents a literature review of the behavior of
individual herbicides tested under a variety of different field and
laboratory conditions. The summary of this literature review presented
below attempts to make some generalizations about each herbicide.
Also presented below is an explanation of the physical characteristics of
herbicides that indicate their potential for contaminating groundwater.
In Appendix II, the discussion of the mobility and persistence of each
herbicide ends with a table of characteristics for that herbicide which
indicate its potential for contaminating ground water. The
characteristics chosen as indicators are those suggested by the Hazard
Evaluation Division (HED) if the Office of Pesticide Programs, EPA, in a
memorandum (June 7, 1983) prepared for use by the FIFRA Scientific
Advisory Panel. Before presenting the data on the individual
herbicides, the following discussion briefly introduces each of the
indicators and the thresholds suggested by HED.
Indicators of the Potential for Ground Water Contamination
Water Solubility The amount of material that will dissolve in water may
be the most critical information about a herbicide regarding its potential
for mobility, since it is a major determinant of how much material wiU
be picked up and carried by water moving through the soil system.
Solubility is expressed in a number of ways; the HED memorandum uses
parts per million, which for these purposes can be considered
equivalent to the number of milligrams of material which can be
dissolved in a liter of water. The threshold value suggested by HED is
30 ppm, a relatively low solubility, so the threshold is a conservative
one. Most of the herbicides in this report are more soluble than this
by one or more orders of magnitude.
Soil Adsorption Coefficient (K ,) .. , , ^. „ ,,. ,
d_ K,, also known as the Freundlich
isotherm, or distribution coefficient, is a parameter that indicates the
-42-
amount of material which is adsorbed onto soil particles. Indirectly, it
indicates the ability of a soil to retain the material. To use the K , to
indicate how much material is retained in soil, the following simple
equation can be used:
V = (1 + 4K ,) to (1 + lOK ,)
d d
V
c
that is, the rate of movement of (V) will be faster than the rate of
movement of the contaminant (V ) by a factor of (1 + 4K ,) to
c ■" a
(1 + lOK,). To put it in a more useful way, if K, = 1, then the
material will move 5 to 11 times slower than the water or will be
retained by a factor of 5 to 11. (Technically, this is true only if
adsorption is rapid and reversable, and if the log-log relationship
between solute concentration and adsorption is linear.)
The HED threshold of K, less than 5 is a conservative one, since it
implies that the herbicide must move at least 21 to 51 times slower than
the surrounding water to be considered as having a low potential for
mobility. Some textbooks suggest a K, threshold of less than 1 as an
indication of mobility. This threshold may not be sufficiently conserva-
tive, considering the slow degradation rates of some of these herbicides
and the amount of water that moves through the surface layers of soil
in New England. A K , value of 3 may be suitably conservative.
This report does not include the K, value as a mobility indicator,
choosing instead to use the K value explained below. The difficulty
with using a K , value is that it varies considerably with soil type. An
individual herbicide may have K , values ranging from 1 to 6, depending
on the type of soil used in the test. This is due to the fact that the
ability of a material to be retained or adsorbed by a soil depends
heavily on the amount of colloids (organic matter and clay), among
other factors, as dicussed above. Using a soil that is high in organic
matter will result in a higher K , value for a herbicide than using a soil
that is low in organic matter. In this report, K, values have been
included where available as part of the discussion of the literature
regarding the fate of the individual herbicides in soil.
-43-
I
K (Kj Divided By the Organic Carbon Content) , j 4. ^ * •
PC d In order to factor m
the adsorptive capacity of the soil, the K is used instead of the K ,.
Dividing the K, by the organic content of the test soil serves to
narrow the range of values obtained, thus providing a more distinctive
set of values for an individual herbicide. For instance, an herbicide
that has a K, of 6 in a soil with moderate organic matter (2%) , and a
Kj of 1.5 in a low organic matter soil (0.5%), would have a K of 300
d oc
in both soils. For the purpose of this report, therefore, it is more
reliable to use a K value than a K , value, given the wide variability
in Massachusetts soils.
It should be noted that K disregards variability in clay content which
can contribute to retention of a herbide. The actual retention may be
higher or lower than the
and type of clay present.
higher or lower than the K value suggests, depending on the amount
WW
The threshold values for K suggested by the HED memorandum are
oc °° ^
conservative. HED appears to have assumed a soil organic content of
1%. Although this is a low organic content, it may reflect conditions in
many parts of the state with poor soils. It also may reflect the sharp
drop in low organic matter commonly found just below the soil surface
in some areas of Massachusetts.
Only a few K values, which were determined from actual soil studies,
■' oc
were found for the herbicides discussed in this report. Most of the
K values in Appendix II were calculated from octanol-water partition
coefficients using a method proposed by Hassett et al. (1979).
Speciation An important factor in the ability of soils to adsorb
herbicides is the type of charge the herbicide has in the soil solution.
If it dissociates in such a way as to form a positively charged ion, it is
called a "cation"; if it dissociates to form a negatively charged ion, it
is an "anion"; if neither, it is referred to as neutral. Most of the sites
available for adsorption in the soil (i.e., the organic matter and the
clay) are negatively charged; thus they attract and hold the positive
cations. Herbicides that are in the form of negatively charged anions
-44-
tend to be repelled by and move quickly past these adsorptive
surfaces.
Although soil pH has a modifying influence as (explained previously),
the statement can generally be made that herbicides which act as
positively charged cations in soil solution are considerably more likely
to be held by the soil than either neutral molecules, or anions.
Herbicides that act as anions in soil solutions are generally the least
likely to be retained by the soil, and therefore are the most likely to
be mobile. In accordance with this generalization, the HED memorandum
suggests that a potential indication of mobility is the dissociation of the
herbicide to form a negatively charged anion.
The speciation of a molecule (i.e., whether it acts as an anion, a cation,
or a neutral molecule) is difficult to determine, because most organic
molecules can act as two, or all three, different forms depending on the
pH of the soil solution. In the preparation of this report, information
about the speciation of the herbicides was generally not available in the
literature or provided by the manufacturer. To give an indication of
the likely speciation, a soil pH of 5 (common to Massachusetts soils, see
Appendix I, Chapter 6) was chosen, and then the structure of the
molecule was examined for the number of likely sites for the gain or
loss of hydrogen protons. After considering the available information
on pK 's for each of the herbicides (pK 's indicate the pH values at
a a
which a change in the amount or type of charge takes place), an
estimation was made of the likely species. Where pK information was
not available, no attempt was made to designate species.
Hydrolysis and Photolysis Half-Lives and Vapor Pressure Compared to
the above parameters, these three indicators are of minor importance.
The hydrolysis half-life generally estimates the amount of chemical (as
opposed to biological) degradation that may occur. The photolysis
half-life estimates the breakdown of the herbicide by sunlight or UV
radiation. The literature review presented in Appendix II indicates
that for almost all the herbicides the primary mechanism of degradation
is by microbial action, and that loss due to chemical degradation and
-45-
photolysis is insignificant compared to loss due to microbial degradation.
Information on hydrolysis and photolysis, however, is included where
available.
Volatilization (as measured by vapor pressure) is also not generally
significant in determining the total amount of herbicide that can move
through the soil. Like photolysis, its importance drops once the
herbicide moves into the soil, where the soil spaces quickly become
saturated. Movement upward may occur slowly at a rate determined by
the volatilization from spaces contiguous to free air above the soil.
Lateral movement of herbicides in the soil by volatilization has not been
extensively studied, but is considered to be insignificant. The HED
memorandum does not provide a threshold for vapor pressure; this
-2
report uses a value of 10 mm Hg.
Soil Half- Life The information conveyed by a soil half-life is not always
clear. In a field study, it can represent the dissipation of the
herbicide by all routes of loss over time. With a herbicide that is
tightly retained by soil, for instance, a half-life measured in the field
very likely represents the degradation of the herbicides. For a highly
mobile herbicide, the half-life may represent the time required for the
herbicide to move vertically or laterally out of the sample site.
Laboratory studies are also unclear, because information on losses due
to mobility may not be provided.
Because of this uncertainty, and because soil half-lives vary so greatly
with soil type and other factors, information on soil half-lives is not
included in the list of mobility indicators, but rather is presented in
the discussion of available literature. Presenting the soil half-life data
as part of a general discussion also allows the description of available
parameters such as soil type, moisture, temperature, and pH, which
may be important in the interpretation of the half-life.
-46-
Summary of Mobility and Persistence Data
Aminotriazole More than other herbicides, the mobility of aminotriazole is
dependent on the adsorptive capacity of the soil. This means it can be
expected to be mobile in sandy soils, but immobile in soil with high organic
matter or high clay content. Aminotriazole has a low to moderate persist-
ence, with half- lives ranging from 6 to 42 days.
Ammate Limited data suggest that Ammate may be mobile in soil. Insuffi-
cient information is available to estimate persistence, or the factors which
affect persistence or mobility.
Atrazine Although conflicting data are available, atrazine can be consid-
ered to have low mobility in soil. Factors which increase mobility include
low organic matter and higher temperature, moisture, and pH. Runoff of
atrazine may occur if a heavy rainfall follows application. Atrazine can be
considered a persistent herbicide, with significsmt residues remaining after
1 to 2 years.
Bromacil Although the mobility of bromacil is significantly affected by the
percentage of organic matter, bromacil can be considered highly mobile in
a number of soils. Bromacil is a persistent herbicide, with a half-life of 3
to 8 months.
2,4-D The available data do not allow a general statement to be made
regarding the mobility of 2,4-D. Important variables seem to be the form
of the herbicide (acid, salt, or ester) and soil factors, particularly the
amount of organic matter. Surfactants also increase mobility. Most avail-
able studies show that 2,4-D is a non-persistent herbicide with a half-life
of less than 2 weeks. Monitoring studies have detected 2,4-D in surface
water samples. In water, 2,4-D may be stable for several months.
Dicamba Studies show dicamba to be highly mobile in soil. Factors which
increase mobility include decreased organic matter and increased pH,
although dicamba' s high mobility makes these factors less important than
they may be for other herbicides. Runoff is not expected to be signifi-
cant, because of the propensity of dicamba to move downward in soil. The
persistence of dicamba in the field is difficult to assess, because of the
rapid dissipation which occurs after rainfall. In the laboratory, dicamba
has a half-life of 4 weeks.
-47-
Diquat Studies show that diquat has low mobility in soil since it is held
tightly by clay and organic matter at the surface of the soil. This strong
adsorption tends to decrease the rate of degradation. Because of this,
diquat is expected to have a long persistence time, although no half-life
values are avciilable. In water, diquat is quickly adsorbed to sediments
and suspended matter and is taken up by aquatic plants. After being
adsorbed by sediments, diquat may persist for several years.
Diuron Available data indicate that diuron is a low-mobility herbicide that
stays near the surface of the soil. Lateral movement also appears to be
limited. Although conflicting results are available, mobility appears to
increase with decreasing organic matter and clay content in soil. Diuron
appears to have low to moderate persistence, with residues disappearing
after 4 to 8 months. In water, diuron is adsorbed onto suspended and
bottom sediments.
Glyphosate Studies show that glyphosate binds rapidly and tightly to
soil particles, and has very low mobility. Mobility increases with
decreasing clay, organic matter, and increasing phosphate, Na+ and Ca-H-
concentration in the soil. Persistence is variable (half-lives range from 3
to 133 days) , probably due to the different adsorption capacities of soils
used the tests. In water, glyphosate appears to be adsorbed to suspended
and bottom sediments and slowly degraded by microorganisms.
®
Krenite Because of a strong tendency to adsorb to soil particles, Kren-
®
ite has a low mobility in soil. Mobility increases with decreasing organic
matter and clay content in soil. Because of its tendency to stay near the
®
soil surface, it may be transported by runoff. Krenite has a low persist-
ence in soil, with a half- life of one week or less.
Metolachlor Available data suggest that metolachlor can be considered
highly mobile in soil. Mobility increases with decreasing organic matter in
soil. Although no data are are publicly available, a review of registration
material by EPA concluded that metolachlor may be persistent in soil (i.e.,
that it has "a potential for long-term environmental stability").
Picloram Studies show that picloram can be considered mobile in soil. It
has a low tendency to adsorb to soil particles . Mobility increases with
-48-
decreasing organic matter, with increased pH, and with increasing concen-
trations of hydrated oxides of aluminum and iron. Runoff studies have
indicated that picloram is likely to move in water as it flows over the soil.
Numerous studies have shown that picloram is moderately to highly persist-
ent, with half-lives of 1 to 13 or more months. Picloram appears to be
less persistent in water than in soil.
Tebuthiuron Studies suggest that tebuthiuron is mobile in the soil.
Because of its tendency to move with water, factors which affect the
mobility of other herbicides have less of an effect on tebuthiuron . It is
very persistent, with half-life values ranging from 4 months to 17 months.
Triclopyr Available data suggest that triclopyr is a mobile herbicide.
Mobility increases with decreasing organic matter. It can be considered
moderately persistent, with half-life values ranging from 46 to 156 days.
EFFECT ON NON-TARGET ORGANISMS
Herbicide use on rights-of-way affects the ecosystem by removing part or
all of the vegetation. The extent of the impact will depend on the selectiv-
ity of both the herbicides and the method of application. On railway
yards and lines, herbicides with a broad range of target species are
"broadcast" over the right-of-way. The effect, therefore, is to eliminate
the vegetative community that would have developed there, and to decrease
the amount of food and cover that would have been provided to animals by
that vegetation.
On utility rights-of-way, herbicides with narrower ranges of effectiveness
are applied to small areas and fewer plants. The impact, therefore, will
be considerably less than that on railroad rights-of-way. On utility
rights-of-way, removal of one component of the vegetative community will
give a competitive advamtage to other vegetation. For instance, studies
have shown that the broadcast spraying of a herbicide that kiUs broadleaf
plants (such as 2,4-D) results in the replacement of those species by
grasses, sedges, ferns, and a few herbicide-resistant shrubs (EPRI,
1978) . A more selective treatment (one that kills trees but avoids damage
to surrounding desirable species) would encourage the spread of the
-49-
surrounding species by increasing the available light, nutrients, and
moisture. Over time, the continued selective removal of trees will
theoretically result in a dominance of desirable species forming a stable
vegetative community that is resistant to invasion of trees. This sub-
ject is discussed in greater detail below in regard to biological control.
Herbicide treatment on both utility and railroad rights-of-way may kill
rare or endangered plants. This is somewhat less likely on railroad
rights-of-way, because the harsh conditions of the ballast or yard area
generally allow the introduction of only common, hardy weed species.
On utility rights-of-way, rare plants are more likely to be found, and
their elimination could result away from the unintended movement of
herbicide from the target plant. A list of rare plants likely to be
found on Massachusetts rights-of-way is provided in Appendix I, Chap-
ter 7, along with a suggested method for inventorying rare plants to
allow them to be a marked on maps and avoided by applicators.
A number of studies have been conducted to assess the effects of
herbicide use on animal communities on rights-of-way. Brambel and
Byrnes (1972) reported a species-specific response to herbicide
spraying as shown in Table 6. Squirrels and rabbits seemed to prefer
the type of treatment likely to cause the least disturbance to
surrounding vegetation, i.e., winter basal treatment. Turkeys, on the
other hand, increased dramatically in response to the treatment that
caused the most disturbance (i.e. broadcast). No clear negative or
positive response to any of the treatments was noted for deer and
grouse. All treatments in this study were conducted with 2,4-D and
2,4,5-T between 1953 and 1957.
Another study by Bramble and Byrnes (1982) showed that favorable
wildlife conditions developed after a series of herbicide applications.
Frtiiting shrubs, such as blueberry, huckleberry, blackberry,
dewberry, and witch-hazel, provided wildlife with food and cover.
EPRI (1978) found that there were no significant differences between
old field communities and the plant communities on utility rights-of-way
mciintained with herbicides in regard to the number of preferred food
plants. The same study conducted a songbird census and found that a
-50-
TABLE 6
NUMBER OF TIMES COMMON WILDLIFE SPECIES OR SIGNS WERE OBSERVED
ON AREAS TREATED WITH 2,4-D AND 2,4,5-T
Treatment
Deer
Turkey Squirrel
Rabbit
Grouse
Unsprayed
83
0
6
51
12
Winter basal
59
1
11
25
8
Summer basal
53
1
8
12
5
Semi-basal
62
1
6
3
7
Broadcast
45
31
2
8
8
Source: Bramble and Byrnes (1972).
large number of species used powerline corridors for nesting, cover,
feeding, and perching.
Herbicides may cause negative effects on animals by altering the chemi-
cal composition of the plants. For instance, they may make desirable
species less palatable, or undesirable species more palatable (Richter,
1952) as cited by Pimentel (1971). Also, harmful contaminants may be
found in plants treated with herbicides. Swanson and Shaw (1954)
concluded that Indian grass concentrated more hydrocyanic acid after
herbicide treatment. The potential for these and other effects on
specific plants depends to a large extent on the chemical properties of
the individual herbicide.
The information presented below summarizes the available information on
the effect of the individual herbicides on non-target organisms likely to
be found on rights-of-way.
-51-
Summary of Data on Toxicity to Non-Target Organisms
Aminotriazole appears to be non-toxic to birds and fish, and slightly
toxic to bees. Soil microbial activity may be inhibited by its
application. Aminotriazole is not likely to bioaccumulate.
®
Ammate appears to be non-toxic to birds and fish, although only
limited data are available. One study shows it to be non-toxic to deer.
®
Ammate may temporarily inhibit soil microbial activity.
Atrazine appears to be non-toxic to birds and livestock. It appears to
be toxic to some species of fish and non-toxic to others. Some lower
aquatic organisms appear to be sensitive to atrazine. In aquatic
ecosystems, atrazine decreases the rate of photosynthesis of some algae,
and, perhaps indirectly, reduces populations of zooplankton. Atrazine
may concentrate to a limited extent in fish, algae, snails, and fungi.
Soil microorganisms show variable responses to atrazine.
Bromacil appears to be non-toxic to birds, fish, lower aquatic organisms
and bees, although only limited data are available.
2,4-D appears to be non-toxic to birds. Its toxicity to fish and aquatic
invertebrates varies with formulation and species of fish. Mammalian
wildlife do not appear to be adversely affected by 2,4-D, except in
response to changes in vegetation caused by its application. Little
adverse effect is observed after exposure of livestock, bees, or soil
organisms to 2,4-D. It does not appear to bioaccumulate in a variety of
terrestrial and aquatic organisms tested.
Dicamba appears to be non -toxic to birds and livestock. It appears to
be moderately toxic to fish, depending on the species. Dicamba
appears to be toxic to a number of aquatic organisms, although data are
contradictory. Dicamba can be considered non-toxic or only slightly
toxic to bees. Limited data suggest that dicamba does not harm soil
microorganisms .
-52-
Diquat appears to be non-toxic to birds. It appears to be toxic to
some species of fish but not to others. Aquatic invertebrates seem to
be able to tolerate diquat, except for amphipods, which are very-
sensitive. Cattle may be somewhat sensitive. Diquat does not
accumulate in fish tissue.
Diuron appears to be non-toxic to birds. No information was found on
the toxicity of diuron to fish. A number of phytoplankton are sensitive
to diuron. One study suggests that diuron inhibits microbial activity in
a number of soils.
Glyphosate appears to be non-toxic to birds , although limited data are
®
available. Roundup appears to be toxic to a number of fish, although
it appears to be the surfactant, not the glyphosate, that causes the
®
mortality. The surfactant used in Roundup is also more toxic than
glyphosate to lower aquatic organisms. Glyphosate appears to be
non-toxic to bees and soil microorganisms. It does not accumulate in
fish tissue.
®
Krenite appears to be non-toxic to birds, fish, lower aquatic
organisms, bees, and soil microorganisms. It does not accumulate in
fish tissue.
Metolachlor appears to be non-toxic to birds and moderately toxic to
fish. Limited data are available.
Picloram appears to be non-toxic to birds and toxic to some species of
fish. It appears to be non-toxic to lower aquatic organisms, livestock,
bees, and soil microorganisms. It does not accumulate in the tissue of
livestock or fish. However, it does accumulate in some fungal species.
Tebuthiuron appears to be non-toxic to birds, fish, lower aquatic
organisms, bees, and livestock,
Triclopyr appears to be non-toxic to birds, fish, and lower aquatic
organisms, although limited data are available on the effect on this last
group of organisms.
_c;-j_
MINIMIZING THE EFFECTS OF HERBICIDES
As is evident from the above discussion, individual herbicides differ
considerably in their potential for impact. The most important way to
minimize impact, therefore, is to choose chemicals with the lowest
potential for adverse affects. A later section which discusses policy
recommendations considers this choice of chemicals in more detail. This
section will discuss ways of minimizing impact that apply to all
herbicides. Many of these are mentioned in other parts of the report,
and are repeated here along with other commonly recommended in the
use of herbicides.
- Protective clothing, including gloves and rubber boots, should
be worn by applicators. (Goggles or other protective eye-wear
should be used when mixing Garlon 3A , because of its acute
eye toxicity). Clothes worn by applicators while spraying
should be washed separately from other clothes,
- Containers should be triple-rinsed and disposed of properly.
They should never be reused, even after thorough washing.
- Spill contingency plans should be prepared, and the equipment
and material necessary for clean-up should be assembled (see
Appendix I, Chapter 5).
- Rights-of-ways should be surveyed for sensitive areas including
streams, adjacent gardens, playgrounds, and campgrounds.
Rights-of-way should be marked, as recommended in Appendix I,
Chapter 4, to alert the applicators of the proximity of these
sensitive areas.
- A survey of wells (as recommended in Appendix I, Chapter 2)
should be conducted, as well as an inventory of rare plants (as
recommended in Appendix I, Chapter 7). Applicators should be
trained to recognize rare plants they might encounter.
-54-
- Access to the right-of-way should be restricted after herbicide
application, especially when the areas are known to be
frequented by berry or mushroom pickers. (A study should be
conducted to determine ways to restrict access, and the
appropriate duration of restricted access after spraying various
herbicides.) Methods should be developed for marking berry
producing plants that are next to target plants receiving
treatment.
- Thickeners and other means of controlling drift should be used.
In the summer, treatment should be restricted to morning or
evening hours to reduce the movement of volatile herbicides.
- To minimize the potential for contamination of ground water and
surface waters, particular attention should be given to the
choice and use of herbicides in areas that may enhance their
mobility. As explained above, these include areas with steep or
long slopes, exposed bedrock, or soils with coarse textures or
low organic matter.
The suggestion has been made to minimize impact by reducing the
frequency of herbicide applications. This idea is worth further study
in regard to railroad yards and lines, where herbicides are applied
every year. Because of the pending regulatory questions, spraying
has been suspended in some areas for the past 1-2 years. During the
course of this study, visual inspection of the areas that have not been
treated showed some encroachment of vegetation along the sides of the
right-of-way. Occasional plants were seen on the ballast near the
track. Although no surveys were made, the intrusion of vegetation
appeared to occupy less than 5% of the area normally sprayed. This
slow invasion of vegetation suggests that applications might be made
every two years instead of every year, without jeopardizing the safety
of railroad operations. An objection has been raised that the decreased
frequency of treatment would allow additional vegetation, including
deeper-rooted perennials, to invade, requiring increased amount of
herbicides for their removal. However, the amount of herbicides used
-55-
every other year would have to be more than twice the usual amount
applied, to outweigh the benefit of decreasing the frequency of the
application to every other year. Given that railroads currently have a
higher rate of application (in pounds of active ingredient) than any use
of herbicides in Massachusetts (except highway vegetation control) , it
is unlikely that this already high rate would have to be increased by
more than a factor of 2 to control the additional weeds. Studies
comparing the effects of applying herbicides every year and every
other year should be conducted to determine the total amounts of
herbicides needed over time.
On utility rights-of-way, decreasing the frequency of herbicide treat-
ments is not likely to decrease the total amount of herbicides used over
time and may even increase it. On utility rights-of-way, the total
amount of herbicides used is determined by the number of trees that
invade the right-of-way. Assuming the treatment is effective, each
tree receives one treatment. Theoretically, the same amount of herbicide
would be used over time if treatments were made — for example every
three years or every five years. This assumes that the frequency of
application has no effect on the number of trees that invade over time.
In fact, visual observation suggests that rights-of-ways that were
treated every five to six years (due to budgetary constraints) resulted
in a greater number of invading trees than rights-of-way that were
treated more frequently (every three to four years) . The explanation
for this may lie in the importance of competition from desirable species
in the inhibition of tree invasion. With the additional growth that occurs
between treatments, larger trees take up more light, nutrients, and
moisture than younger, smaller trees. Over time, eliminating the trees
with more frequent herbicide treatment may decrease this stress on the
surrounding desirable species and allow the surrounding vegetation to
become increasingly able to resist tree invasion.
-56-
PHYSICAL ALTERNATIVES
The alternative to herbicide use in the control of vegetation on
rights-of-way is the use of physical means of killing vegetation,
including chainsaws, larger cutting machines, and fire. The following
section presents each of these and discusses their advantages and
disadvantages .
Handcutting
Cutting trees with chainsaws is the most common alternative to herbicide
use in controlling trees on Massachusetts rights-of-way. This practice
involves severing trees near the base, and then cutting the tree into
sections that can be piled nearby. (Sometimes the stump is then
treated with herbicides to prevent sprouting). Girdling is another way
of using axes or chainsaws. Girdling involves making shallow cuts
around the trunk to disrupt the flow of nutrients to the roots. Chain-
sawing also involves trimming trees that interfere with sight lines or
wires on railroad rights-of-way. Most trimming involves removing side
branches of trees that extend into the right-of-way area.
The advantage of handcutting is that it avoids introducing chemicals
into the right-of-way and the surrounding environment. Another
advantage is the degree of selectivity that can be achieved; with
careful cutting using small chainsaws, surrounding plants suffer
minimum damage. A further advantage is that handcutting prevents
contact with wires when trees are at dangerous heights.
The disadvantages of handcutting are:
1. High cost (discussed in more detail below in the comparison of
alternative control measures) .
2. The failure to control trees that sprout rapidly. Many trees in
Massachusetts, including oak (one of the most common) are
capable of sprouting from cut stumps. Handcutting of these
trees results in an increase in the number of stems per acre.
-57-
Because of the rapid growth of these sprouts, handcutting may
have to be done every year.
3. The serious hazard to workers. A survey of workers by
Vegetation Control Service, Inc. (conducted for this study)
noted 36 cuts from chainsaws during the period of 1976 to 1983,
based on worker's compensation data for a total of 21
employees. Cuts to the leg, knee, hand, and head numbered
12, 14, 9, and 1, respectively. Causes of chainsaw accidents
include loss of balance while using the saw, skidding and
bounding of the saw, and extended follow-through of the saw
after severing the tree trunk. "Kickback" is also a major cause
of accidents. Kickback is the sudden movement of the saw
upward and back toward the operator due to some interference
with the movement of the chain. Steep slopes are a
contributing factor in chainsaw accidents, and handcutting is
not recommended on slopes greater than 30%. Wet conditions
also increase the likelihood of accidents.
To minimize the hazards associated with handcutting, proper handling of
the chainsaw is necessary. Important considerations include:
Starting and maintaining all cuts at full throttle;
staying clear of the path the saw will follow on completion of
the cut;
- adjustment of the throttle speed so that the chain does not
move when the engine is idling;
- starting the saw when it is on the ground (i.e., no "hip
starts").
Recent technological advances have resulted in chainsaws that are
considerably less likely to kickback. However, it is likely that even
with proper handling and new technology, the potential for serious
accidents will continue to be high.
-58-
Mechanical Cutting
The use of larger machinery to cut vegetation on utility rights-of-way
includes :
Pushing , or uprooting the trees with a tracked vehicle equipped with
a push bar; the debris can be removed or left for slash disposal. Erosion
controls must be used because of the severe disruption of the soil.
Scalping, or scraping off all plants and the top layer of soil. This
method can be used only with young trees. Erosion control measures must
be used and a considerable amount of valuable soil will be lost. Either
wheeled or tracked vehicles Cein be used. On gentle slopes with few
rocks, wide moldboard plows are sufficient. On steeper slopes, the blade
should be mounted on a hydraulic hitch to allow raising or lowering. An
adjustable bulldozer blade can also be employed if it is used with care.
Discing cind plowing, or cutting and turning over vegetation and soil.
A variety of conventional tillage implements can be used. This method
scarifies the soil, so erosion control measures must be used. Only young
trees can be removed by this method.
Roller chopping , or forcing shrubs and trees to the ground and cut-
ting them into small pieces. Pulled over an area with a tracked vehicle, a
roller chopper pushes the tree and cuts it with a blade mounted on heavy
metal drums filled with water. Trees up to 6 inches in diameter can be
removed by this method. Because it does not intentioncdly disrupt soil,
erosion problems will be less severe with this method than with other
mechanical methods. Because the vegetation is cut up immediately, prob-
lems of disposal and site appearance will be considerably lessened also.
Sheardozing, or severing all stems close to the ground. Although
this method causes soil disturbance by uprooting some vegetation, disturb-
ance can be minimized by waiting until the ground freezes before sheardoz-
ing. Stems up to 10 inches in diameter can be removed by this method.
Brushraking and root raking, or scraping up brush and roots and
removing cut material. A tracked vehicle is used with a specially designed
toothed blade that uproots and removes brush, and a cutting bar attached
to the bottom of its teeth to sever roots below the soil surface.
Mechanical cutting on the ballast area on a railroad right-of-way is not
possible, because both above and below ground biomass must be kiUed
-59-
without disturbing the ballast itself. Control of trees and shrubs on the
side of the track can be done mechanically, however, using a high-rail
vehicle especially designed as a brushcutter with large cutter heads
mounted on flexible arms that can sever trees up to 14 inches in diameter
and cut a swath up to 28 feet on both sides of track centerline.
The benefit of mechanical cutting on both utility and railroad rights-of-
way is that it avoids the introduction of chemicals to the right of way
while it decreases the danger to the operator imposed by handcutting tools
such as chainsaws. The disadvantages of mechanical cutting, however,
include other safety problems caused by the use of machines with large
cutting blades. The railway brush cutter may be particularly dangerous
in this regard. .With its 7-foot cutting blades rotating at very rapid
speeds, vegetation and other matericd with which it comes into contact are
likely to spin off in all directions. Personnel must walk the tracks along
with the vehicle, staying out of range of the flying material but close
enough to be able to warn people who may be near the right-of-way. This
machine may pose a particular hazard to children in urbem areas who may
use the railway as a play area, as well as those in rural areas who may
use the railway as a path to follow through wooded areas. When a brush-
cutter was tried in Massachusetts, area residents complained about the
adverse aethetic impact of the cut area and the lack of privacy resulting
from the complete removal of vegetation.
Another disadvantage of mechanical control on both railroad and utility
rights-of-way is its failure to control trees that are capable of sprouting
from cut stumps. As explained above in regard to handcutting, mechanical
cutting results in an increase in density of stems per acre.
On utility rights-of-way, another major disadvantage of mechanical cutting
is the lack of selectivity in vegetation removed. Even on rights-of-way
with a low density of trees, mechanical cutting results in damage to large
areas of vegetation, especially since many of these machines leave a swath
of damage as they move from one target tree to the next.
Other problems with mechanical control include erosion of soils after
removal of vegetation and adverse aesthetic impact. Erosion problems
occur with scalping, plowing, and other methods that disturb the soil.
-60-
Adverse aesthetic impact can be expected from mechanical methods; they
tend to leave an area looking "bombed out."
Fire
As a control alternative, fire eliminates trees and if done periodically,
it tends to maintain a low growth of vegetation. Many species that are
desirable on rights-of-way spread by underground stems or roots and
are able to tolerate fire. Controlled burning has been tried
successfully on rights-of-way in New Hampshire (Dr. David Olson,
University of New Hampshire, personal communication, 10/6/83).
Several experiments are underway to test the efficacy of burning on
rights-of-way at different times of the year.
Prescribed burning is done in four steps: planning, site preparation,
burning, and mopping up. Planning involves tactical preparations and
notification of appropriate authorities and local inhabitants. Tactical
preparations include deciding upon the necessary weather and soil
conditions, planning the direction of the burn and the placement of fire
lines, notifying back-up forces in case the fire gets out of control, and
planning insofar as possible the strategies to be used should the fire
escape.
Part of site preparation includes the clearing of fire lines on either side
of the right-of-way. Fire lines are strips at least several feet wide
that are cleared of all organic material down to mineral soil. A power
line right-of-way would probably require one line on each outer edge
and periodic lines crossing the right-of-way, so that the area can be
burned in blocks instead of in one long strip, which is harder to
control. The necessary width of the fire line must be calculated on the
basis of the height, density, and moisture of the vegetation to be
burned.
A common way to ignite fires is to use a drip torch, which drips
lighted fuel onto the vegetation. (Another method which is not
recommended is to ignite the burn with a "Heli-Torch, " a helicopter
used by the Forest Service which drops flaming balls of napalm onto an
-61-
area to be burned.) A standard practice is to start the fire at the outside
edges of an area, and allow the burn to move towards the center, thereby-
extinguishing itself due to lack of fuel. To mop up afterwards, workers
must return to the site within hours or days after the fire and check for
smoldering remains.
Hatnd-operated weed burners can also be used as an alternative to herbi-
cides on utility rights-of-way. These high-intensity torches, also called
flame guns, consist of a fuel tank pressurized with a hand pump connected
to a hose, with a steel tube coil and spray plug which serves as a burner
head. A small amount of fuel drips into the coil, where it is heated until it
vaporizes and produces a flame similar to a blowtorch. The tree trunk is
girdled by the flame, destroying the conductive tissue along the perimeter
of the trunk. The method has been shown to be effective on white pine,
red maple, sugar maple, birches, aspen, red oak, white ash, and shagbark
hickory. The advantages of this method are that it can be used year-round,
and it is less costly than cutting the tree or girdling it mechanically. It is
particularly efficient at treating sprout clumps, since the flame easily wraps
around such smaller stems. Young or thin-barked stems are lethally damaged
in 10 seconds or less, while larger stems or thick-barked trees require 20
seconds or more. The disadvantages of this method are: (1) it does not
control trees that sprout, and (2) it cannot be used in dry weather or
under other conditions of fire hazard.
On railroad rights-of-way, controlled burning was used historically to clear
vegetation (to reduce the chance of accidental fires from steam engines) . A
current method for burning ballast areas is to use a track burner, a high-
rail vehicle that runs on the tracks and has two arms, about 15 feet long,
which extend perpendicularly to the tracks. These arms carry propane
torches which burn the vegetation. The torches are so hot that the vegeta-
tion itself does not have to carry the fire, so the burning can be done in
relatively wet weather. This method requires two or three people on the
truck and two or three people to control the fire.
The advantages of controlled burning as a vegetation control technique are
that it avoids the use of herbicides and, at the same time, favors the
establishment of desired herb and tree species that resist tree invasion.
Additionally, prescribed burning at appropriate intervals will reduce
buildup of fuel, (i.e., flammable plant material). This can be especially
-62-
important in dry, sandy areas, such as Cape Cod. Over the years, both
mechanical and chemical control can lead to a build-up of dead plant mate-
rial on the right-of-way, resulting in a potential fire hazard which would be
eliminated by a controlled burn.
The disadvantages of controlled burning include the following:
1. The greatest danger, of course, is the escape of fire. Controlled
burning is usually done in large areas surrounded by a buffer of uninhab-
ited land that could absorb a wildfire. The rights-of-way in Massachusetts
constitute narrow strips of Icind, often in urban and surb urban areas,
without such buffer zones.
2. Power may be interrupted. In some controlled burns, the Forest
Service recommends shutting off the power in transmission lines that cross
the area to be burned. This prevents electrical discharge between the
lines or between the lines and the grotind, sometimes caused by the ionized
particles in the smoke which can carry the charge.
3. The conditions needed for safe but efficient burning are restric-
tive. The moisture of the vegetation and soil must be low enough to allow
sufficient combustion, but high enough to avoid burning \inderground
rhizomes and soil organic matter. Air temperature and wind patterns must
also be appropriate, and the best conditions for smoke dispersal may be the
worst for the escape of the fire. Thus, there may be very few times of
the year when conditions are appropriate.
4. Aesthetic impacts are another potential problem along rights-of-way
that are viewed frequently by large numbers of people. Vegetation does
enter burned sites quickly, but even a few months of looking burned-over
may create sufficient public disapproval to restrict the use of fire.
5. Air pollution is a problem, as fire smoke contains particulates,
nitrous oxides, ozone, carbon monoxide, and gaseous hydrocarbons. The
high amounts of particulates can also restrict visibility near highways.
Other Physical Methods
A suggestion has been made to use physical barriers under the ballast on
rights-of-way to prevent emergence of weeds. This approach would be
ineffective, since airborne seed introduction and build-up of debris from
introduced leaves and other organic matter would still allow weeds to
develop. Periodic additions of extra ballast has also been suggested, but
this method is prohibitively expensive (it costs a minimum of $5000 /mile to
upgrade ballast) and would need to be done about every four years.
-63-
BIOLOGICAL CONTROL ON RIGHTS-OF-WAY
Biological control is an attempt to control unwanted organisms by in-
creasing the populations of their natural enemies and competitors.
Based on an understanding of the ecology of the unwanted organism
and its surroundings, effective biological control increases the
pressures exerted by its natural enemies and competitors, thus keeping
the population of the unwanted organism at low levels. The following
section examines this concept as it relates to vegetation control on
utility and railroad rights-of-way. Appendix I, Chapter 3, provides
more detail on a number of topics discussed in this section.
Control by Natural Enemies
Biological control has classically involved the introduction of an
antagonistic species, such as the introduction of the nucleopolyhedrosis
virus for the control of gypsy moth. For plants, antagonistic species
fall into two groups, grazers and disease agents. A suggestion has
been made that grazers, e.g., goats or deer, could be introduced to
rights-of-way for vegetation control. The difficulties and limitations in
this approach are too numerous to enumerate, but include an inability
to assure effectiveness, and a substantial cost and effort to keep the
grazers on the rights-of-way.
A more practical approach, at least theoretically, is the introduction of
plant pathogens. In natural systems, a number of tree species
occasionally suffer high loss to wilts and other diseases caused by
fungi. Severe dieback of ash has been achieved in nursery studies
when the trees are inoculated with a pathogenic fungus. However,
even though potentially lethal pathogenic fungi exist for all the tree
species likely to be found on rights-of-way, the approach is not yet
practical for a number of reasons. One reason is that most tree
diseases usually do not kill all, or even most, of their host species.
Most host plant species and plant diseases have evolved together to
form a stable long-term association. In this association, neither species
is likely to eliminate the other in a particular area — either by
-64-
destruction of all the trees by the fungus or by complete resistance of
the plant to the fungus. Thus, increasing the population of an
indigenous pathogenic fungus would not be sufficiently effective in
controlling trees on the right-of-way.
It may be possible to introduce a pathogen that has not yet evolved to
form a stable association with its host species, and thereby potentially
kill most of the trees on a right-of-way. The obvious problem with this
approach is that anything that would kill a significant number of trees
on the rights-of-way would also kill a significant number of trees in
adjacent and surrounding areas. The Dutch elm disease, caused by an
introduced fungal pathogen to which the elm had no resistance,
provides an example of the rapid spread and large-scale decimation that
can occur upon the introduction of a pathogen. Because fungi are
easily disseminated in the environment by wind, water, and insects, it
is unlikely that the introduced pathogen could be contained within the
right-of-way.
On railroad rights-of-way the introduction of antagonistic species is
even more limited. The goal of vegetation control on railroad
rights-of-way is to eliminate all vegetation. No super-pathogen exists
that will kill cdl species of plants. Conceivably, between 10 and 100
different species would need to be released, increasing the danger of
the fungi spreading to adjacent areas beyond the right-of-way.
The suggestion has been made to use a certain kind of fungi that would
kill young seedlings and have a wide host range (hundreds or thou-
sands of hosts) , as a supplement to using herbicides or other means of
control. These fungi (which cause "damping off" of seedlings) could be
introduced to the railroad bed to prevent new seedlings from estab-
lishing in the cleared area. However, the extensive inoculation,
throughout the Commonwealth, of a fungus with such a wide host range
is bound to endanger local agriculture. Furthermore, these fungi grow
best in moist, crowded conditions, which are not likely to be found on
railroad rights-of-way.
-65-
Control by competition
Biological control also includes the regulation of unwanted organisms by
an increase in the competitive pressures exerted by surrounding
organisms. Although this concept is not applicable to railroad ballasts
where all species must be eliminated, it may have considerable
importance in controlling vegetation on powerline rights-of-way and in
brush control on railroad rights-of-way.
Encouraging competition on rights-of-way means promoting and
maintaining the growth of so-called "desirable" species, i.e., low
growing shrubs and herbaceous plants, to the exclusion of trees.
Normally, shrubs and herbs are dominant only for a limited time, being
gradually replaced by trees. This "succession" involves a gradual
change in vegetative communities, leading eventually to a "climax"
community of trees that is able to maintain itself over time. Appendix
I, Chapter 3, contains a discussion of the various theories which have
been advanced to explain and predict succession, and how these
theories may relate to the control of vegetation on rights-of-way. In
theory at least, biological control can be accomplished if the pre-climax
species (shrubs and herbs) can become a stable vegetative community
successfully preventing the invasion of trees.
Stable vegetative communities have been identified by a number of
researchers. Niering and Egler (1955) reported a stand of Viburnum
lentago in southwestern Connecticut that had no tree invasion for at
least 25 years. Niering and Goodwin (1934) identified communities of
witch hazel, speckled alder, sheep laurel, and other species in various
parts of Connecticut that appeared stable to tree invasion for up to
several decades. In another study, a fire line was cleared and
harrowed through a southeastern New York forest between 1934 and
1936. In one segment, a complex of stable tree-less communities
(including ferns, sedge and, bushes) resisted tree invasion until at
least 1953 (Pound and Egler, 1953). Horsley (personal communication,
9/8/1983) described a power line right-of-way in Pennsylvania that had
been sprayed with herbicides once 40 years ago, after which a
-66-
community of ferns developed. Tree seedlings germinated in the
community, but the seedlings did not emerge above the fern cover.
Mechanisms that may be responsible for the resistance to tree invasion
in these examples include the following:
1. Soil conditions that are unfavorable to trees but are tolerated
by a number of shrubs and herbs; e.g., heaths may inhibit
tree invasion by the buildup of acid duff in the soil;
2. Grazing, e.g., deer browsing of young trees;
3. Periodic fires;
4. Allelopathy (the production of chemicals by one plant that are
inhibitory to the growth of another plant); and
5. The "head start" provided by a pre-existing or rapid buildup
of a high density of shrubs and herbs, particularly those that
can spread by underground stems.
Herbicide applications and /or mechanical cutting are often cited as
mechanisms to inhibit tree invasion. On the surface this idea may seem
to be somewhat circular, i.e., that tree invasion can be prevented by
the removal of trees. However, it appears that tree removal may give a
competitive advantage to desirable species by decreasing the moisture,
light, and other stresses imposed by the trees. Over time, this may
promote an increasing density of desirable species, which may in turn
result in a slow decrease in the invasion of new trees. Appendix I,
Chapter 3, presents examples in which periodic chemical treatment
significantly decreased tree invasion over time.
A number of species commonly found in Massachusetts have been found
to be components of stable shrub communities. A brief discussion of a
number of these species, including sheep laurel, witch hazel,
blueberry, goldenrod, little bluestem, and others is included in
Appendix II, in Chapter 3. A common characteristic of these plants is
an ability to grow in a variety of conditions including low-nutrient soils
and wet or dry habitats.
-67-
In the preparation of this report the following treatments (and their
limitations) were identified that may be used to promote the growth of
desirable species and limit tree invasion:
1. Planting indigenous species Some species are limited in abun-
dance by a low density of seeds, and would benefit by the addition of
seeds to rights-of-way. Blackberry, for example, can form a dense
cover following disturbance if its seeds are present in sufficient
numbers. If there are only a few seeds, it can take much longer to
reach a high density (Bramble and Byrnes, 1982). These authors make
a more general statement that species which produce abundant seeds at
the right time (for example, witch hazel which produces seeds in the
fall) often become prominent in the stable shrub communities.
Experts disagree on the efficacy of planting along rights-of-way.
Egler and Foote (1975) state that this approach is impractical because of
the amount of care that would be needed to maintain the introduced
plants. On the other hand, Littlefield produced a list of species
appropriate for planting on rights-of-way, including viburnums, bristly
locusts, hawthorns, hawkweed, fireweed, and ferns (L. Littlefield,
personal communication 10/3/83). Tilman (1976) planted several species
of plants on a southeastern New York right-of-way.
Because of the expense involved, it wouljd probably not be practical to
introduce whole plants. Introduced species should be restricted to
those that can be seeded and which do not require soil manipulation or
great care. The simplest technique is to broadcast seed (perhaps little
bluestem) along a right-of-way during the time in which trees are being
mechanically or chemically removed. More intensive plantings might be
possible in small, ecologically sensitive areas as an alternative to
mechanical or chemical control.
2. Soil amendments A logical approach would be to amend the soil
to make it suitable to desirable species. However, there are several
difficulties with this approach:
-68-
- Soil treatments that are of benefit to shrubs and herbs are
often of benefit to trees as well. For example, fertilization to
benefit bracken fern may also encourage oak.
Often, the principle components of stable shrub communities are
species that tolerate poor, acid soils. These species might lose
their dominance if soil conditions were "improved" by additions
of fertilizers or lime.
Soil treatments that favor one set of desirable species may
hinder another. For instance, some desirable grasses, such as
little bluestem, can be encouraged by liming. However, liming
can damage several desirable shrubs such as blueberries,
mountain laurel, and sweetfem, which prefer acid soils.
3. Use of symbiotic fungi Certain kinds of soil fungi called
"mycorrhizae" form symbiotic association with plant roots. In these
associations, the plants provide the fungi with simple sugars while, in
return, the fungus provides the plant with the phosphorus that it
absorbs from the soil. Plants that enter into mycorrhizal relationships
are often able to grow faster and out-compete plants that are not
associated with mycorrhizae. To some extent, different types of
mycorrhizae are limited in the hosts that they can infect. Three types
of mycorrhizae are of interest in regard to rights-of-way:
TYPE OF MYCORRHIZAE ASSOCIATED PLANT SPECIES
Ectomycorrhizae Oak, beech, alder, pine,
spruce, hemlock.
VA (vesicular-arbuscular) Maple, cherry, sassafras,
ferns, most herbs and shrubs.
Ericoid Blueberry, huckleberry, lau-
rel, azalea, rhododendron.
Since VA and ericoid mycorrhizae infect primarily desirable species
(except for maple, cherry, and sassafras) it is conceivable that
-69-
desirable species could be given a competitive advantage by increasing
the concentration of these mycorrhizae. At present, however, it is not
possible to produce large enough quantities of innoculum of VA or
ericoid mycorrhizae to consider adding these to the soil at levels above
those that naturally occur there. Abbott Laboratories and Monsanto
Chemical Company are both attempting to produce large amounts of
VA-mycorrhizae, but costs are prohibitive. For example, a 1-quart
container of spores (in soil) , sufficient to cover less than 100 square
feet of soil surface, costs approximately $25. Another limitation is the
lack of information regarding application techniques that will ensure the
success of the mycorrhizae in the field.
4. Fire Many species that may be able to resist tree invasion are
favored by fire. These species, which include little bluestem,
sweetfern, huckleberry, and sheep laurel, tend to appear on
burned-over sites soon after a fire. Many of these species are colonial,
that is, they spread by underground or above-ground stems or roots,
which partially explains their ability to remain alive during fires and to
sprout afterwards. One way of encouraging species resistant to tree
invasion, therefore, may be to periodically burn the right-of-way. The
benefits and limitations of controlled burning have been discussed
previously in this report. The conclusion of that discussion was that
the hazards associated with burning limit its use on rights-of-way.
Research in this area is currently underway, however, and the pos-
sibility exists that controlled burning may yet be a means for encour-
aging desirable species as well as removing trees.
5. Planting commercial crops So far, this investigation has evalu-
ated treatments from the point of view of minimizing cost and effort.
However, use of the right-of-way to grow commercial species can also
be considered a form of biological control. Utility rights-of-way can be
used for pasture, farmland, or wood production. Blueberries, for
instance, may be grown in areas with acid soils. Wood production can
include trees grown for boards and Christmas trees, and for
reconstituted products, including paper and particle board. A pilot
study on wood production along Maine highway rights-of-way indicates
-70-
that such an effort could be profitable within a few years (Hatton, 1982).
On utility rights-of-way, disadvantages of growing commercial crops include
the logistical problems of access and that, for some crops, the use of
chemical control agents would be greater than that currently used.
Conclusions Regarding Biological Control
A number of reviewers of the draft GEIR felt that the report was not
sufficiently enthusiastic about biological control. The draft concluded that:
1) Biological control is not a viable option for maintaining a vegeta-
tion-free area on railroad rights-of-way. A vegetation-free area is not a
natural biological occurrence, and therefore it is difficult to find and
exploit a biological mechanism for its maintencince.
2) A greater chance of success for biological control may be possible
when considering powerline rights-of-way. Competition from desirable
species should be encouraged as a biological mechanism for decreasing the
need for biological control. Selective removal of undesirable species, by
either chemical or mechanical means, can be supplemented by the addition of
seeds of desirable species, improving soil conditions, and growing commer-
cial crops where conditions permit.
The above statement regarding biological control on powerlines should have
been more strongly worded in spite of frequent admonitions throughout the
report to use competition from desirable species as the basis for any control
effort on powerlines. This report strongly recommends biological control
when it is defined in this sense; i.e., as control by competition. The term
"biological control" was not used because this approach usually is based on
the use of non-biological methods; that is, the selective chemical or mechan-
ical elimination of the undesirable species as the means to achieve control
by competition; and use of the term is therefore confusing, and "control by
competition" or "encouragement of desirable species" should be used instead.
Again, this report strongly recommends a biologically based control of
undesirable vegetation on utility rights-of-way by competitive pressure
exerted by desirable species. It also recommends the elimination of undesir-
able species by chemiccil or mechanical means as an important element in
achieving control by competition. Once this is achieved, further need to
eliminate undesirable species by mechanical or chemical means should be
minimal or nonexistent. This biologically based approach should be an
integral part of both utility and railroad (brush control) efforts.
-71-
INFORMATION REQUESTED BY REVIEWERS
The review of the draft GEIR resiilted in a number of requests for addi-
tional information. Some of that information has been integrated into other
sections of this report. This section presents the remainder of that infor-
mation as a series of short discussions.
Additional Information on Utility Practices
Information on the practices of the three major utilities (which maintain
about 90% of rights-of-way in Massachusetts) is presented in the following
tables. The first table shows the active ingredients used, the types of
application, and the mixtures used. The second table, provided by New
England Power Co., indicates which active ingredients are potentially usable
against which trees.
Railroad Practices
Additional information was requested on the vegetation control practices of
railroads ; namely ,
1) How many applicators operate in Massachusetts? Two applicators
control vegetation on rsdlroads in the Commonwealth : Railroad Weed Control
Inc. of Westfield, Massachusetts, and Asplundh, Inc., of Willow Grove,
Pennsylvania.
2) How many track miles are treated with herbicides? In 1983, 780
miles were identified as needing treatment, 480 miles were treated. The
remaining 300 miles were not treated, due to proximity to water bodies.
3) What is the frequency of treatment on various segments of track?
All track in Massachusetts is treated on an annual basis.
4) What mixtures of herbicides are used, and how often are they
used? Mixtures are used in 100% of ballast control efforts. Preemergent
treatment, done on 65-70% of the track miles, involves mixtures of atrazine
and diuron. Postemergent treatment, done of 30-35% of the track miles,
involves mixtures of atrazine, diuron, glyphosate, and sometimes metolach-
lor. Brush control is often limited to the use of glyphosate alone.
5) How often is manual or mechanical control used, and what railroads
use this type of control? No manual or mechanical control is done on
72
w
u
(— i
H
u
<
CU
H
H
D
Q
Q
1
1
r-^ rji
1
n) .
^ '^'T:
W M
§
CO
fS rsj E
>>
C!
'o >H
O t!
■g
«»
' -H .tj
^
Jh pc3
CL
s
S G^
o
0
•T^ 0 T3
2
0 0
(0
U
<u v« 5
2; o *«
1
••-1 H
0
1
!h 0
CQ
Ui H
HH
(0
(4
CO
(U
(U
J3
4-»
0
•1-1
2 D|
>>
T3
fi
a
1— •
s
&o
o
&
O
u
^
<u
(U
^
2:
0
cu
E
o
E
3
.y CO
-3
1
E a
QO
rt T*
-^3
«4H H c
1— 1 •<-> c
3 CO <u
. "
"^.tS
^ '
§3'
lopy
mba
E
3
•s ' ^
u
^
;3
mmo
ate
reni
• iH
1-H
U (Q
•«->
0
•S.i:}
CO
VM
H Q
< ^
Q
I
o h
O
Q
I
'St*
(V3
o\«> OP o\o
O ITl LO
O rH I— I
o^o 00 o\o
r^ o^ <Nj
I I I
i-H vO i-H
0)
I c^'S 13 o ^
I
S u V. p:J « CO < ,
2 ^ S . §g ■ [3
t»i! Eh H O
a»3 a^
I
CO
o
w o
a
a
o
m
o\o dP o\o
un If) in
>• (M
Q
1 "^
(N3 E ^^ E
>— I O f_, o
2 'y cci '^
' ' a^rf ^*^ .^
o
u
o
H
c
o
O
H
(U
o
«= 75 "
H
o
S
0)
o
c«
0)
o
S
4)
+»
4)
a
(0
(0
4)
is
e
o
u
4>
o
o
C
{«
X
i
m
fl O
0)
.f-l Q)
4) n» g
^ ^ u
to ^
9) S
< O
CO 3
(J
^ ^^
^ -C S
4)
CO
a
CO
4)
■*-»
X
•rH
2
0)
o
S
(0
o
4)
&o
4)
u
<
>
•l-t
u
■H
^ 0)
U o
2
I
I
SO
>
•ft
■♦J
u
<u
%
>H >
<u "^
^ o
O 4)
SO
0)
ay ■«-»
SO
>
•♦-*
u
0)
4) >^
>
4^
O
(4
<a
^
MH
0)
-a
0
1
s
^
1
3.^
m
m
SO
4>
.>:
u
VM
0)
I— I
U >
^ o
O 0)
"5 ^<-t
-« t^
I
SO
>
o
M^ «j 4) 4)
2 >H > C
1 O _(U '
2 , w
(0
en
en
>-« <TJ CTJ (rt
►^ SO c/3
4)
>
^
■!-•
>
u
•iH
w
4)
w
4;
4>
> «
^t5
w
4)
w
4)
a^
a^
rt rt
rt nj
s 0
SO
w
z
w
>
1—1
H
U
w
fa
W
Q
t— <
U
w
4)
>
•i-t
4) -M
I
4)
I
(n
<
U
CO
4;
o
CQ O
4)
c
u
•fH
PL4
o
a.
o
X
4) V
>^
^ (0
4} CO
4)
>> o
4) c
4)
T3 I
O
S CO
en O
<o
4)
>
4) •*->
0) 4)
4) ^
4)
Oi u
•■g-Ss
VM 5 '
VM "^
w , 2
en .S O
< « "
U
en
<
>
•M
■H
CJ
4)
«M
VM
0)
4)
4;
4;
O
S
4;
>
• M
•4-»
o
4) w ,
O
4)
VM
VM
W
u
u
en
4)
o
CQ U
a.
u
■<-»
•M
o
VM
a
4J
U
!3
00
0)
U
4)
c
o
I
' VM
•M
^ c
en o
4)
>
•IH
4)
VM
VM
4>
4)
O
S
u
4)
VM
VM
w
I
4)
>
4J
o
4)
■»-> 4) 4)
<.M .i^ r^^
4>
4;
>
4) .s; I
U
4)
VM
VM
4>
4;
4J
4;
O
S
en .2
< pa
u
I— 1
CQ
O U
CJ
en
4)
c
o
CQ U
4>
u
«
VM
VM
0)
>^
I— I
4}
♦J
4) h
- o o
tt 4J S
O VM
<0 VM ,
en
4>
u
I
en
<
o
o
CQU
<0
>
•M
4J
4)
4) ^
> 4>
9)
I
' M-l
• M
en o
<o
••
D
••
• •
1-1
Eh
0
0
0
pe;
c>a
fVJ
1— 1
r-
in
A
fi
l-H
«-H
0
0
4)
$
'0
TS
>
>
»4
V4
a
q
0
0
rt
(i
H
H
CQ
m
en
u
pq
4)
fi
•M
E
cei
en
o
fa
4)
n)
en
o
a
>>
r— I
o
a
o
ballast by any railroad in Massachusetts. Large (e.g., Conrail) and
small (e.g., Providence and Worcester) railroads use both manual/
mechanical controls and herbicides to control brush. No clear informa-
tion is available on the amount of brush control that involves only
herbicides or only mechanical or manual effort; responses to questions
in this regard were that herbicides are often used as a followup treat-
ment after mechanic cil/ manual control.
6) Is the use of fire currently an alternative in Massachusetts?
Apparently, there has been no use of ballast burners in Massachusetts,
although equipment is available. The equipment is similar to highrail
vehicles used for herbicide application, with propeine torches in place of
sprayers. These torches provide a very hot, quick burn which is not
likely to smoulder and spread to adjacent areas. Cost data were not
available, although railroad sources stated that costs would be "prohib-
itive." The National Railway Association could not name any manufac-
turers of this equipment nor any railroad that used it. The National
Railway Association stated also that control by fire could not be used in
any state which prohibited open burning, including Massachusetts.
7) Why are such high rates of herbicide application used in
vegetation control on ballasts? No data were found that justified the
use of current rates of application. The need for such rates is highly
questionable .
Highway Practices
A number of comments on the draft GEIR requested additional informa-
tion on use of herbicides on highways; specifically, those comments
from
MEPA
Department of Public Health
Town of Belmont
Cambridge Water Board
Massachusetts Association of Conservation Commissions
Nashua River Watershed Council
Cape Cod Planning and Economic Development Commission
The process by which decisions are made at MDPW regarding vegetation
control is as follows. Each of the eight Districts of the MDPW has
a district road-maintenance engineer who inspects highways for
75
maintenance problems. This person identifies areas that need treat-
ment, specifies the type of control (e.g., manual cutting or a specific
herbicide) that should be used on that particular vegetation problem,
and estimates the cost for the treatment problem. The Maintenance
Division at MDPW headquarters reviews these requests and allocates
portions of the total MDPW funds available for vegetation control to the
individual districts. Since materieds for vegetation control are pur-
chased by the Maintenance Division before the start of the application
season, it is likely that there is an estimation on the amount of treat-
ment and the herbicides to be used on a statewide basis with input from
the districts.
An inquiry was made at MEPA's request into the status of aminotriazole
(including Fenavar®, which cont«dns aminotriazole) at the Massachusetts
Department of Public Works (MDPW) , given the evidence of carcinogenic-
ity presented in the draft GEIR. The Maintenance Division of the
MDPW stated that it would not be used in the next fiscal year (summer
of 1985) because of the decision on the part of EPA to restrict the
chemical (thereby requiring applicators of aminotriazole to be certified
in right-of-way maintenance) .
Prometon
Although originally considered for inclusion in this report, prometon
was dropped from the list. Ciba-Geigy is not marketing prometon for
right-of-way use since it recognizes there are more cost-effective
alternatives. According to a company spokesman, prometon has not
been used for right-of-way use in Massachusetts for a considerable
time, and they do not expect any significant use in the future. It is
still registered for use on rights-of-way.
Outline for Long-range Management Plan
The following is a brief outline of the important steps in assuring
minimal need for vegetation control when creating a new right-of-way.
76
The utility plan presents the important activities of the first 10-12
years. The railroad plan takes a different approach, discussing mate-
rials which could be added to the ballast upon creation of the right-
of-way, or with more difficulty, at a later stage. The ideas presented
for utility rights-of-way were generated by the author in a previous
study (Arthur D. Little, Inc., 1979). The ideas presented for railroad
ballasts, however, were generated by the author without benefit of
sufficient previous study. No written material or current research was
located on the ideas presented.
Utility rights-of-way and brush control along railways
Purpose ; To increase competitive pressure exerted by desirable
species and thereby decrease the need for vegetation control.
Methods: 1) Maximize sunlight penetration (most undesirable
species are shade-tolerant, whereas desirable ones often are not); 2)
chemically kill roots of any undesirable trees capable of sprouting; 3)
seed or plant desirable species or increase their density through soil
manipulations .
Plan; 1) Overeill approach is to give the desirable species a good
start by paying close attention to the right-of-way in the first five
years. After 10 or 12 years, the right-of-way should approach stabil-
ity and require minimal effort because of a low density of undesirable
species .
Specific Approach; Year 1: Clearcut to maximize sunlight pene-
tration .
Year 2: Chemically treat stump of any trees capable of sprouting.
Years 3-5 : Deplete seedbank of undesirable trees by cutting or
spraying (should be done yearly or every other year to prevent seed-
lings from shading desirable species). Also seed, plant, or otherwise
encourage desirable species.
Years 6-12: Treat every three years to deter invasion of exogen-
ous seeds. Continue to chemically kill roots of sprouting trees.
Year 12 Onward; Monitor eind cut or treat every three to five
years as necessary. Need for control (stems /acre) should decrease
slowly .
77
Ballast of railway
Purpose; To deter plant invasion, to prevent soil buildup, and to
remove plants as they appear.
Methods: 1) Generate inhospitable conditions for plants by adding
materials to the surface of the ballast which increase stress on plzints;
2) decrease the rate of soil generation through the addition of materials
which deter microbial degradation; 3) remove vegetation manually or by
fire or chemical treatment as necessary.
Plan; The overcdl approach is to discourage seeds from germinat-
ing on the ballast. It is important to prevent the plants from invading
so that subsequent soil buildup does not occur. Soil buildup greatly
accelerates the further invasion of plants by providing favorable sites
for seed germination. Currently, this preventative effort has been
based on the use of preemergent herbicides. The alternative suggested
here is to prevent invasion by making the ballast more inhospitable;
i.e., more stressful to plants, and by decreasing the rate of organic
decomposition which precedes soil buildup. If vegetation appears, the
vegetation would be removed and additional efforts to slow organic
decomposition would be made.
Specific Plan ; Add materials to the ballast which would increase
plant stress, such as a) adsorbants and chelators, e.g., activated
charcoal and EDTA, respectively, to compete for nutrients; b) absorb-
emts, e.g., silica gel particles, to compete for moisture; c) amy black
material, e.g., low-grade coal, to increase surface temperatures.
Closely monitor the ballast for plant invasion and remove as necessary.
The most effective means of removal would be manual, if care were
taken to remove as much of the root system as possible. While costs
for manual removal would be prohibitive if done by the railroads them-
selves, cooperative agreements with towns to maintain the track acreage
within that town could be a source of economical labor. A number of
such agreements have recently been made between towns and utilities to
mainteiin powerline rights-of-way. Particular attention must be paid to
the issue of safety when considering similar arrangements on rsdlroad
rights-of-way .
78
If manual removal was not possible, treatment with fire or herbi-
cides would be necessary. If herbicides were used, it is possible that
spot treatments may be sufficient. Instead of using a conventional
sprayer which distributes material across the entire track, spot treat-
ments could be done as they are on utility rights-of-way; i.e., applied
by individuals using sprayers connected to a vehicle carrying herbi-
cide. At a place needing treatment, one or more individuals could
direct the sprayers at the invading vegetation. Since most of the
invading vegetation encroaches slowly from the sides of the ballast,
selective treatment of these areas may alleviate problems which fre-
quently trigger a treatment of the entire ballast.
Because removal by fire or herbicide would leave much of the
organic material remaining, efforts must be made to slow organic decom-
position leading to soil buildup. Some of the stress-inducing agents
(adsorbants, chelators, heat absorbers, etc.) would also deter microbial
activity. Additional deterrence should be provided by adding a slow-
release bacteriastatic material similar to those in many household prod-
ucts. This should be done along the entire ballast, even in areas
without plant invasion, because of the buildup of leaves, spores, and
other organic materied deposited on the ballast.
The long-range plan would be to add more stress-inducing and
bacteriastatic material, and remove vegetation only as necessary. The
frequency of these various activities is difficult to assess because this
approach has yet to be tested. Several years of testing will be neces-
sary to see if this approach; i.e., eliminating the need for preemergent
herbicides by making the ballast less conducive to plant invasion and
by decreasing organic decomposition, will be an effective means of
controlling vegetation.
Synergism
A number of reviewers expressed concern about the interactions of
herbicides with each other and with other man-made compounds. Those
who expressed such concern included:
79
Department of Public Health
Towns of Belmont, Somerville, and Plain ville
Massachusetts Association of Conservation Commissions
Vietnam Veterans of America
University of Massachusetts Cranberry Station
Citizens for Safe Use of Pesticides
Citizens Pesticide Council
Massachusetts Audubon Society
Goodwin, Proctor, and Hoar
Lindsay Martuci
Michael Rosebury
The toxicity of two chemicals used in combination can sometimes be
roughly predicted from the relative toxicities of each alone. The acute
oral LD 50 of Tordon 101, for example, is 3080 mg/kg in rats. The LD
50's for 2,4-D and picloram, individually, are 375 mg/kg and 8200
mg/kg. Such an interaction is termed 'additive.' Sometimes, however,
the interaction results in an unexpected increase or decrease in toxic-
ity. An increase in toxicity occurs when an interaction is 'synergistic,'
a decrease in toxicity occurs when an interaction is 'antagonistic'
Predicting the result of exposure to more than one chemical is difficult
because of the complexity of possible interactions within the body.
When the body is exposed to a chemical, a series of chemical reactions
controls the amount and rate of input to the body, transport and
storage within the body, metabolic breakdown, excretion, and the
adverse effect at the target site, if any. Two chemicals may interact
synergistically or antagonistically when they affect the same set of
reactions at any of these stages of response. The magnitude of the
synergism depends on the importance of that set stage of bodily
response as a limiting factor in the toxicity of either of the chemicals.
For example, if one chemical is limited in its effect primarily by its
inability to pass through the skin, and another chemical increases the
absorptive capacity of the skin, a significant synergistic effect may be
observed. However, if the first chemical was limited in its effect by
enzymatic degradation, something which increased the absorptive capac-
ity of skin would have much less of an effect.
One of the difficulties in predicting interactive effects is due to a
change in limiting factors associated with chajiges in age, sex, and
80
physiological condition of the organism. Thus, at one time, the organ-
ism may be able to metabolize a herbicide, while at a more advanced
age, without a full set of necessary enzymes, the organism must rely on
tissue storage for protection. At this later time, a synergistic inter-
action could result from an exposure to a second herbicide competing
for tissue-binding sites.
A frequent type of interaction occurs when one herbicide affects the
enzymatic activity responsible for metabolizing another. Furthermore,
this enzymatic activity is often the limiting step in determining the
response of an organism. These interactions can be particularly diffi-
cult to predict, since:
1) either chemical may increase or decrease the numbers and kinds
of available enzymes,
2) the enzymes affected may either detoxify or activate one or
both herbicides,
3) the sequence and timing of the exposure to the herbicides can
determine which enzymes are affected and whether they are increased
or decreased by the interaction.
This last complication arises in part from 'induction' of enzymes; i.e.,
exposure to a herbicide may trigger the induction of enzymes which are
capable of metabolizing it. If the induced enzymes are non-specific
(e.g., the hepatic microsomal oxidase enzymes, which are important in
the oxidation of a wide range of foreign compounds) , the organism may
more quickly metabolize another herbicide upon exposure. In this case,
the interaction would be antagonistic. Timing is critical, however,
since induction of the important enzymes may not occur until hours or
days after exposure to the first chemical, or only after chronic expo-
sure. Timing can also be important when one compound inhibits an
enzyme after an accumulation of metabolic products. Necessary enzymes
may not be available upon subsequent exposure to another chemical.
Lastly, if the exposure is simultaneous, competition for existing enzyme
binding sites can occur, leading to a temporary increase in toxic
response if the enzyme system is overloaded. The effect in this case
will depend in part on the relative affinities of the two chemicals for
binding sites.
- 8-1 -
Interactions which occur at the target receptor (i.e., the cell which
iiltimately is harmed by the toxin) are less common than those which are
involved in absorption, distribution, and metabolism. At the target
receptor, many interactions are competitive, since the harmful effect of
various toxins is often similar. The interaction, therefore, is commonly
antagonistic. Exceptions can occur when two compounds act differently
on a single system. A well-known example is the exposure to organochlo-
rine insecticides, which cause hyperexcitability and increase the neuro-
transmitter acetylcholine, and organophosphate insecticides, which
increase the acetylcholine by preventing its degradation by cholines-
terase.
The effect of herbicides on sensitive populations can be considered a
type of (potentially) synergistic interaction. Instead of interacting with
another chemical, however, the herbicide interacts with conditions of
the body which increase its susceptibility to the herbicide. Sensitive
populations may include people who are HI, taking medication, pregnant,
old, dieting, malnourished, and those with genetic traits that impair
their ability to tolerate foreign compounds. Some reviewers suggested
that all humans should be considered members of a sensitive population.
Since the limiting mechanisms which enable the body to tolerate individ-
ual chemicals cire not well understood, and because these limiting mecha-
nisms may change with the individual and his physiological condition,
the suggestion to consider all humans as sensitive has merit. However,
the need still exists to consider a category of people who may be more
susceptible to herbicides than others.
Effects of herbicides on sensitive populations has received little
attention. Most toxicological studies are designed to test the effect of a
chemical on normal, healthy organisms. A great deal of attention is
given to assuring that laboratory organisms are not in a weakened state
which might predispose them to show a harmful effect. The most
conservative test for toxicity, however, would use subpopulations which
are particularly vulnerable to harm. These subpopulations would have
to be defined for each chemical based on the particular response of the
organism to that chemical. Sensitive organisms would be those that
had:
_ 82
1) an increased likelihood of absorbing the herbicide,
2) a decreased ability to detoxify or excrete the compound,
3) an increased sensitivity of the receptor site, and
4) a decreased ability to tolerate the effect at the receptor site.
Unfortunately, the number of physiological states which would contrib-
ute to these sensitivities are too numerous to test. At best, a thor-
ough risk assessment will identify the numerous diseases or genetic
impairments which involve the receptor site affected by the particular
compound being studied.
Any information located in the course of this study on the potential
synergistic interactions of the fourteen herbicides and their effects on
sensitive populations is included in Appendix II,
Degradation
A number of reviewers stated that insufficient information was provided
on the degradation of herbicides .
Degradation of herbicides proceeds by a variety of mechanisms, such as
microbial or chemical degradation and photolysis. Microbial degradation
is probably the most important in the breakdown of the fourteen herbi-
cides addressed in this report, especially once the herbicides reach the
soil.
Bacteria and fungi in the soil will break down the herbicide molecule in
a series of steps which often begins with such simple changes as the
removal of a hydroxyl group and proceeds to more difficult steps such
as the cleavage of a ring structure. Numerous microbial species are
usually involved in the breakdown of a particular herbicide. A variety
of species are often available which can perform the first, and easiest,
breakdown steps. As the steps become more difficult, degradation
becomes slower and more dependent on the availability of particular
types of microbes, and thus on the particular conditions of the soil.
Ideally, degradation proceeds until the products are those which are
- 83 -
ubiquitous in nature, such as carbon dioxide and water. 2,4-D, for
instance, breaks down completely in a variety of soils into products like
succinic acid normally found in those soils. Most herbicides probably
do not break down this completely, although few have been studied as
thoroughly as 2,4-D. More likely, degradation proceeds until microor-
ganisms capable of degrading them further are not available and the
residue, called a terminal residue, remains as is for a considerable time
in the soil. One common fate of these terminal residues is incorporation
into soil humus or even into the biomass of the microbes themselves.
In the water, microbial degradation occurs in both the water cind on
suspended particulate matter. Since microbial populations in water and
on suspended matter differ, the rates of microbial degradation will
depend to some extent on the amount of particulate material and the
tendency of the herbicide to be adsorbed to the material. The amount
of dissolved oxygen is also important, because it determines to some
extent the microbial populations that will be present in that habitat. It
also determines the type and rates of enzymatic activity since the
activity of many enzymes depends on oxygen availability. Finally,
dissolved organic matter, such as humic acid or petroleum contaminamts ,
is also important because it can change the solubility and availability of
the herbicide. Increased solubility and availability may be kinetically
more desirable since the microbes have access to higher concentrations.
However, concentrations can increase to levels which are toxic to the
microorganisms .
In both soil and water, the ability of microorganisms to degrade a
chemical depends to a large extent on the structure and complexity of
the molecule. There are a few rough 'rules of thumb':
1) Aromatic hydrocarbons (i.e., those with rings) are more diffi-
cult to degrade than compounds made up of chains, such as alkanes.
2) Branched chains are more difficult to break down than straight
chains.
3) Within the aromatics, benzene, a single unsubstituted ring, is
more difficult to degrade than poly cyclic compounds (more than one
ring) or substituted rings (with radicals such as hydrocarbon chains
_ 84 -
attached) . Addition of chlorine significantly decreases the biodegrad-
ability of any ring structure.
The degradation products formed by microbial metabolism or other forms
of decomposition may be substantially different from the parent com-
pound, or very similar. More importantly, they may result in an
increase or a decrease in toxicity. Photodieldrin , a product of both
photo- and microbial degradation of dieldrin, is a well-known example of
a degradation product which is more toxic than the parent compound.
Also, metabolic products can be more toxic than the original compound
after it is activated by enzymatic activity.
As shown in Appendix II, there are often several degradation products
which have been identified for a particular chemical. The toxicity of
many of these degradation products has not been studied. Additional
information in this regard was located during the preparation of the
final GEIR and has been included in Appendix II.
Drift
Some comments on the draft GEIR requested that additional information
be provided on the potential for herbicides to drift. Specifically, the
groups that made this request were:
DEQE Office of Research & Standards
Natural Resources Commission
Smithsonian Institute of Environmental Research
Goodwin, Proctor, and Hoar
Towns of Southampton, Westport, and Plainville
Drift is the movement of herbicide by air currents to locations outside
of the target area. Drift has always been a concern in the application
of herbicides because of the potential injury to plants outside the local
area and because of the potential harm to humans and other organisms.
An important factor in assessing the potential for drift is the particle
size of the herbicide droplet. Droplets above 500 microns are generally
considered drift safe. Using large droplets, however, may result in
- 85
increased amounts of herbicides applied to the rights-of-way, since
smaller droplets facilitate greater coverage per volume of herbicide,
especially in foliar applications. Application equipment often allows the
user to choose the desired droplet size, to the extent that a small
stream of herbicide may be released, rather than a spray. Thickeners
in the tank mix also contribute to the creation of large droplet sizes.
It should be noted that a range of particle sizes is likely to be released
by most equipment, even at settings which increase particle size. The
proportions of different particle sizes, however, will vary.
The vapor pressure of the herbicide and its carrier is particularly
important, since it partly determines the decrease in size of the particle
as it moves away from the target area. A volatile herbicide 10 um in
diameter will take hours to evaporate completely, while a nonvolatile
herbicide of the same size would take months to evaporate. The vapor
pressure of the carrier is also important, since it determines to a large
extent whether the carrier moves with the herbicide or independent of
it. Highly volatile carriers such as kerosene may volatilize quickly and
move large distances in vapor form. Detecting the carrier by smell
therefore may or may not mean that the person is also in contact with
the herbicide . That person would be in contact with both the herbicide
and the carrier if 1) the exposure included droplets as well as vapors,
2) the vapor pressure of the herbicides and the carrier were similar, or
3) the evaporation of the carrier reduced the particle size of the mix-
ture to such an extent that it was entrained in the air and carried with
the vaporized carrier.
Other important factors include weather conditions and types of appli-
cations. The most important weather condition is probably wind, includ-
ing its speed, direction, and turbulence. Temperature is also impor-
tant, since volatility increases with temperature. Humid conditions, on
the other hand, tend to decrease volatility. Sunlight can make a
difference if the herbicide is susceptible to photolysis, since photolysis
can decrease the concentrations in the air as well as on leaf surfaces
where further evaporation could take place after application.
- 86
Types of application are cilso important. Drift is most likely in foliar
application where the herbicide must be sprayed into the air in smaller
droplets than used in other types of application. Dirift is less likely to
occur in basal application where a more directed spray is applied at the
base of the plant. The least chance for drift occurs with cut stump
treatments or the use of pellets, although herbicides may evaporate
slowly over time.
Commonly, damage to vegetation adjacent to rights-of-way is used as an
indication of drift. However, small droplets in a strong or turbulent
wind may result in concentrations of herbicide in air that are too low to
visibly affect surrounding vegetation, even though measurable amounts
may be moving off the right-of-way. The significance of long-range
movements from the target site of low concentrations of herbicide is
unclear. Because herbicides are applied for only a short time and in
a small area, the concentrations of herbicides which will result on a
regional level are probably insignificant. A greater potential for
problems exists in areas close to the rights-of-way where levels too low
to cause visible vegetation damage may be high enough to affect humans
and other organisms. Diquat applications are of particular concern,
since information from Chevron Chemical Company states that "breathing
spray mist may cause nasal, throat, and respiratory tract irritations."
The situation is less clear in regard to the other herbicides. Acute
effects are generally not likely to occur; however, scientific questions
remain concerning the concentrations of a chemical and frequency of
exposure likely to cause long-term effects.
Surfactants
A number of comments on the draft GEIR requested additional information
on inert ingredients in herbicide formulations, specifically adjuvants and
surfactants. An adjuvant is any material which increases the bioactiv-
ity of the active ingredient. Surfactants, also known as surface active
agents, are compounds that reduce the surface tension between two
liquids or between a liquid and a solid. (The term "surfactants" actu-
ally describes two sets of compounds — one which facilitates mixing of
- 87 -
the active ingredient in its carrier and one which increases the contact
and absorption of the active ingredient on the surface of the leaf. In
the first sense, a surfactant accomplishes the same purpose as an
emulsifier . )
Both surfactants and adjuvants are numerous and varied in their chemi-
cal structure. In fact, there may easily be more surfactants in number
than pesticides as a class of compounds. Without knowing the chemical
structure and mode of action, it is difficult to generalize about their
environmental impact, except to say that surfactants are likely to
increase mobility by facilitating the movement of herbicide with the flow
of water. (On the other hand, if the surfactant is designed to increase
absorption by target plants, it may result in less active ingredients
released to the environment.) Reviewers of the draft GEIR were
particularly concerned about bee toxicity; again, it is not possible to
assess this without specific tests for bee toxicity. (Such tests,
however, have been done for diesel oil, another concern of reviewers,
and the carrier has been found to be toxic to bees.) As indicated in
Appendix II, toxicity to fish has been associated with surfactants used
in a glyphosate formulation. As of this writing (June 1984) , Monsanto
is still using this surfactant in its glyphosate formulation.
During the preparation of the draft GEIR, very little information was
found on the toxicity or mobility of the various inert ingredients used
in the herbicide formulations. The Commonwealth does not routinely
require information on the inert ingredients of a herbicide formulation.
Only when a particular herbicide is designated as being of concern will
the Commonwealth decide what additional information is required from
the manufacturer. If necessary, additional information required may
include data on the effects of the inert ingredients in the formulation.
(On a routine basis, the only data required by the Commonwealth to
register a herbicide is a copy of the label, a technical data sheet, aind
a copy of the registration form.)
88
Risk Assessment
In the review of the draft GEIR, a question was raised regarding
whether exposure to these herbicides will result in harm to humans or
other organisms. This question must be answered on a case-by-case
basis .
Given the scope of this report, it is not possible to assess whether
exposure will result in a physiological response. Such a determination
would require an answer to two questions: 1) what amounts of herbi-
cide reach people by various routes of exposure, and 2) would those
amounts trigger a physiological response? The first question requires a
model for each route of transport, shown in Table 5. These models
would have to estimate the amount of herbicide remaining after various
dispersion and degradation mechanisms acted on the herbicide en route
from the site of application. The second question, predicting the
physiological response to the estimated exposure levels, requires
another kind of modeling effort. For the various toxicity tests (chronic
oral, teratogenity, subchronic inhalation, etc.), "no-effect levels" need
to be determined; i.e., the highest dosage level at which no adverse
effects are observed. After dividing by a safety factor (commonly 100
or 1,000), an allowable daily intake level would then need to be deter-
mined for each route of exposure. These levels must then be compared
to the predicted exposure level to determine the probability that a
physiological response might occur.
Data Checklist
Reviewers requested that a checklist of required information be pro-
vided so that new herbicides can be evaluated as they enter the mar-
ket.
The following is a checklist of the types of information which should be
considered when evaluating a pesticide. The list is taken from EPA's
delineation of data, which must be submitted as part of a registration
application. Not all information is required by EPA for every product
or use.
- 89 -
Product Information
Product identity and disclosure of ingredients
Description of manufacturing process
Discussion of the formation of unintentional ingredients
Declaration and certification of ingredient limits
Product analytical methods and data
Physical /chemical properties:
Color
Odor
Melting point
Solubility
Stability
Octanol /water partition coefficient
Physical state
Density or specific gravity
Vapor pressure
pH
Dissociation constant
Flamm ability
Oxidizing or reducing action
Explosiveness
MiscibiHty
Viscosity
Corrosion characteristics
Toxicity
Acute oral toxicity
Acute dermal toxicity
Acute inhalation toxicity
Primary dermal irritation
Dermal sensitization
90-day oral toxicity
21-day dermal toxicity
90 -day dermal toxicity
90-day inhalation toxicity
Acute delayed neurotoxicity
90-day neurotoxicity
Chronic feeding test
Oncogenicity
Teratogenicity
Reproduction
Mutagenicity
-90-
Ecological Effects
Acute avian toxicity
Avian dietary toxicity
Avian reproduction
Wild mammal toxicity
Simulated eind actual field tests on mammals and birds
Acute fish toxicity (warm- and cold-water fish)
Acute toxicity to aquatic invertebrates
Acute toxicity to estuarine and marine organisms
Effects on ecirly life stages of fish
Effects on fish lifecycle
Effects on acquatic invertebrate life cycles
Accumulation in aquatic organisms
Simulated or actued field tests on aquatic organisms
Honeybee acute contact toxicity
Honeybee toxicity of residues on foliage
Wild bee toxicity of residues on foliage
Honey bee subacute feeding toxicity
Field tests on pollinators
Acute toxicity to aquatic insects
Aquatic insect lifecycle effects
Simulated or actual field tests on aquatic insects
Effects on predators and parasites
Target area phytotoxicity
Non-target area phytotoxicity:
Seed germination/ seedling emergence
Vegetative vigor
Aquatic plant growth
Field studies on terrestrial and aquatic plants
Metabolism and Residues
Uptake, distribution, and metabolism in plants
Metabolism in food-producing animals
Domestic animal safety
Analytic methods for residue analysis
Residues in:
Potable water
-91-
Fish
Processed foods
Raw agricultural commodities
Meat, milk, poultry, and eggs
Environmental Fate
Hydrolysis
Photode gradation in water, soil, and air
Volatilization
Aerobic and anaerobic soil metabolism
Aerobic and anaerobic aquatic metabolism
Effects of microbes on pesticide
Effects of pesticide on microbes
Leaching and adsorption/ desorption
Field dissipation in terrestrial and aquatic systems, forests, and in
long-term studies, and as combination and tank mixes
Accumulation in rotational crops (confined and field), in irrigated
crops, cind in fish and aquatic invertebrates
The Regulation of Pesticides in Massachusetts
Several reviewers asked for more information regarding pesticide
regulation in Massachusetts. The following section was written by the
Massachusetts Department of Food and Agriculture.
In order to understand the current pesticide-regulatory scheme in
Massachusetts, it is necessary to take a brief look at the history of the
regulation of pesticides in the United States.
History of Federal Regulation of Pesticides
The U.S. Congress passed the Federal Insecticide, Fungicide and
Rodenticide Act (FIFRA) in 1947. This law gave the mandate for
regulating pesticides to the U.S. Department of Agriculture (USDA) .
The law required federal registration of pesticides suid specific labeling
on each product to facilitate its identification as it was distributed from
one state to the next.
-92-
The requirements for pesticide registration at that time consisted of
efficacy data and some acute and chronic toxicity data.
In 1970, the Environmental Protection Agency (EPA) was formed and
given broad jurisdiction to regulate the presence of chemicals in air,
soil, and water. Part of these duties was to regulate pesticides, with
the mandate coming from two laws: 1) the amended FIFRA (1972 and
1978) and 2) the Pesticide Amendment to the Federal Food, Drug and
Cosmetic Act (FFDCA) .
The amended FIFRA greatly increased the data requirements needed to
support pesticide registration. It also established two categories of
pesticide classification, general use, and restricted use.
General-use pesticides are generally available for purchase by anyone,
and there are no restrictions for use except those specified on the
label. Restricted-use pesticides can only by sold by licensed dealers,
can only be purchased by certified individuals and can only be used by
either a certified individual or someone under their direct supervision.
(The license and certification process is explained below.)
The amended FIFRA also included a mandate to each state for the
development of a state plan to enforce FIFRA and to license /certify
dealers and applicators.
The Pesticide Amendment to the FFDCA established limits (tolereinces)
for pesticide residues in food or feed crops. The tolerances are estab-
lished by the EPA and are enforceable. The monitoring of foods to
ensure compliance is conducted by the Federal Food and Drug Adminis-
tration (FDA) in their Market Basket Survey.
Federal Pesticide Registration Process
1. Registration. The amended FIFRA (1978) requires that registrants
submit certain data to support the registration of any new pesticide
products . These requirements were only recently finalized in
-93-
regulations (40 CRF Part 158, 49 FR 42881, October 24, 1984) and
include data on product chemistry, residue chemistry, environmental
fate, toxicology, reentry protection, spray drift, effects on wildlife auid
aquatic organisms, and more.
The regulations identify documents known as Pesticide Assessment
Guidelines as listing the "... standards for conducting acceptable
tests, guidance on evaluation eind reporting of data, definition of terms,
further guidance on when data are required, and examples of acceptable
protocols." These guidelines are available through the National Techni-
cal Information Service, 5285 Port Royal Rd., Springfield, VA 22161
(703/487-4650).
2, Re-registration . The amended FIFRA (1978) requires that the EPA
review all pesticide active ingredients registered on or before January
1, 1977, through the Registration Standards Program.
"The Registration Standard Program involves a thorough review of the
scientific data base underlying pesticide regulations and an identifi-
cation of essential but missing studies which may not have been
required when the product was initially registered or studies that are
now considered insufficient." (Taken from the preamble of one of the
Registration Standards issued.)
Once the EPA has assessed the data supporting the registration of an
active ingredient, a document is issued (a Registration Standard) which
details the federal regulatory position for the registrations of all
pesticides containing that active ingredient along with the rationale
behind this position.
3. Special Review. This process — formerly known as RPAR
(Rebuttable Presumption Against Registration) — allows the EPA to
consider new information regarding a potential for adverse effect on
human health or the environment of a chemical which has been
registered or reregistered.
-94-
The criteria ("triggers") which must be met or exceeded in order for a
pesticide to be placed on Special Review have been identified in regula-
tions (40 CFR 162.11).
The Special Review process involves three stages and can take up to
several years before a regulatory decision is made.
History of Massachusetts Regulation of Pesticides
The Massachusetts Department of Public Health (DPH) was given
authority to regulate pesticides in the early 1960s through Chapter 94B
of the Massachusetts General Laws. The Pesticide Board was placed in
the DPH in 1962 and was given the mandate to register pesticides and
control the use and application of pesticides. In 1963, the Common-
wealth began a program to license and train pesticide applicators.
The Pesticide Board was moved from the DPH to the newly formed
Department of Environmental Quality Engineering (DEQE) in 1975.
However, the administrative duties concerning pesticide registration
(mail-out of applications, receipt of fees, approving applications)
remained in the Division of Food and Drug of the DPH.
In 1978, in response to the amended FIFRA mandate to states to develop
a state plan to enforce the federal law and to maintain a licensing/
certification program, the Massachusetts Legislature passed the Massa-
chusetts Pesticide Control Act (MPCA, Chaper 132B of the MGL) . This
law placed the Pesticide Board in the Department of Food and Agricul-
ture (DFA) , with the day-to-day work carried out by the Pesticide
Bureau.
Present Pesticide Regulatory Scheme in Massachusetts
Through the MPCA, there are three entities involved in the Massachu-
setts pesticide-regulatory scheme — the Pesticide Bureau, the Pesticide
Board, and the Pesticide Board Subcommittee.
1. Pesticide Bureau. The Bureau has five main functions:
-95-
1) Licensing /Certification Program. The Bureau maintains a pro-
gram to license and/or certify individuals who wish to use pesticides
commercially, sell restricted-use pesticides, or purchase and use
restricted-use pesticides. There are four categories of licensing /cer-
tification .
The process requires that an individual purchase the appropriate
study manual from the Cooperative Extension Service, study it, and
then take the exeim for the license or certification category of interest.
Once the exam has been passed, the individual is eligible for a license
or certification.
2) Enforcement. The Bureau enforces both the FIFRA and the
MPCA by conducting routine inspections and investigations of use/ mis-
use pesticide applications.
Routine inspections include inspecting establishments which manu-
facture pesticides, retail outlets which sell general-use pesticides, and
outlets managed by licensed dealers which sell restricted-use pesticides.
Use/ misuse investigations involve answering consumer complcdnts,
observing pesticide applications by licensed /certified individuals to
ensure compliance with the label and laws, and inspecting the records
of pesticide application at commercial-applicator establishments.
3) Registration. In the Fall of 1982, the administrative duties
surrounding the registration of pesticides was moved from the Division
of Food and Drug (DPH) to the Bureau. Therefore, the mailing out of
applications, receipt and processing of fees, and the approval of
re-registrations only is carried out by the Bureau. (See Pesticide
Board Subcommittee.)
4) Education. As a part of a state agency, the Bureau is obli-
gated to educate the general public on the proper use and handling of
pesticides.
5) Staff to the Pesticide Board and Pesticide Board Subcommittee.
The Bureau provides a variety of support functions for the Board and
Subcommittee.
2. Pesticide Board. Section 3 of the MPCA establishes a Pesticide
Board consisting of 13 members: six ex-officio members representing
-96-
various state agencies, and seven gubernatorial appointees representing
various interest groups.
The Board meets approximately six to eight times a year. The
functions of the Board are to approve of Department (Bureau) regula-
tions and policies and to act as an appeal board for grievances incurred
as a result of Bureau enforcement actions or Subcommittee registration
decisions (see below).
3. Pesticide Board Subcommittee. Section 3A of the MPCA establishes
a Pesticide Board Subcommittee consisting of five members, all of which
are on the Pesticide Board. The five members include four ex-officio
members and one gubernatorial appointee.
The function and responsibility of the Subcommittee is to register
all pesticides distributed, sold, or used in Massachusetts.
Since the Subcommittee only meets between 10 and 12 times a year,
it has delegated to the Bureau the authority to approve pesticide
re-registration applications (those products which were registered the
previous year in the Commonwealth) . New pesticide product registra-
tions are reviewed by the Subcommittee prior to approval or
disapproval.
The Subcommittee is also responsible for registering Experimental
Use Permits (EUPs — permits granted by the EPA to allow the use of a
pesticide to generate data to support an eventual, "normal" registration
application) and Special Local Needs Registrations (SLNs or 24Cs — the
mechanism by which a state Ccin register a use of a product not on the
federal registration of that product to meet a Special Local Need) .
It should be noted that the FIFRA allows states to be more restric-
tive than the EPA regarding the registration status of pesticides in that
particular state.
-97-
EVALUATION OF ALTERNATIVES
The choice of the best alternative for a particular right-of-way segment
depends on a number of conditions, such as
- weather conditions
- season of the year
- difficulty of the terrain
- cost-effectiveness
- potential for impact.
This section presents a discussion of the chemical and physical control
alternatives with regard to these considerations. Biological control is
not evaluated as an cdtemative in this section because, as discussed
above, it is not yet a possible replacement for chemical or physical
alternatives. Fire is also not included in this evaluation because,
again, current research has not progressed far enough to alleviate the
concerns about its use as a control measure in Massachusetts.
Flexibility
Part of the choice of the best alternative involves constraints imposed
by difficult terrain, by particular seasons of the year, and by adverse
weather conditions. Table 7 shows the limitations imposed by these
considerations on such alternatives as hand-cutting and mowing, and
various methods of herbicide application. Information on some of the
more commonly used herbicides is also included.
As shown in Table 7, hand-cutting and mowing (as an example of
mechanical control) are primarily limited by terrain. Hand-cutting with
chcdn-saws becomes dangerous in areas with steep slopes, especially if
they are wet. Mechanical control must have a firm, reasonably flat
surface for operation, and therefore its use is limited in rocky areas,
in areas with soft or wet soils, ledges and steep slopes, and in areas
with stumps. Physical control methods are not limited by season or
weather except by deep snow cover.
The constraints on chemical control methods are often imposed by
weather or season. Foliar sprays, of course, can be applied only
98
w
<
<
W
H
Q
<
o
<
w
w
H
<
CQ
Q
W
W
o
I— I
CO
2
O
<
(U
CO
D
<u
pq
Eh
O
2
2
<
U
c
<u
E
■♦->
0)
u
(U
D
CO
C
O
C
O
U
o
CO
(U
w
CO
(U
CO
■M
CO
rock
es,
4)
^
^
•^
* o
CO 'm
CO
•"^ a.
<u
CO 0)
a
^ <l>
0
w
^ .CO
(U
4->
ISI
/2
§
•IH
o
2
^4
>
o
o
CO
a
Q
S
■M
o
C
r-Hf '^
(U
nl
C
E
O
rt
CO
E
0)
>^
»4
^
H
Om
o
2
•n
G
bO
a
Pi
(0
to
CO
CO
0)
(0
CO OJ
.2
f^r.
•4J
0) (U
n>
(U ^
•<->
-*->
•pH
tn
J
1—1
0
Very i
rocks ,
2
c
•1-1
4-»
c
u
;h
a
(TJ
(U
(U
>^
1^
■♦J
CO
s
C
a
I— 1
l-H
o
■4->
13
Oj
•iH
■M
bO
MH
bo
E
-cH
C
c
(U
•iH
(U
• iH
1—1
•M
^
+J
^
ffj
CU
rt
a
0
J
CO
J
CO
2
o
CO
a,
(0
0)
73
O
C!
CO
Pi
u
>
o
u
'a
X
o
X
T3 o
1-^
o
0
fl) rt
3
(TJ
X
^H a
rt
a
0)
0 "J
>>
o
c
0^ CQ
X
CQ
o
• iH
•♦->
OJ
1
1
o
•iH
;h
l-H
l-H
t— 1
(TJ
(d
C3
a
•r-l
0)
U
.iH
E
<
0
fa
0)
^
U
CO
X
u
> bo
-»-> *
a CO
^ a;
a
C? CO 41
•iH .,H
-a ci^ CO
<H (U ^
fd 1)
<u
C/3 CO ^
u
•iH
td
CO
C
o
.<H
■*-»
•IH
E
.iH
I-H
o
2
bO
rtJ
C!
1— t
•i^
u
C
a
• rH
CO
^
>>
^
r—t
^H
a
(U
03
•k
CO
h
J3
bo
fl
n: ^
i^
o
U
Vi
o
TJ
(0
f— •
00
2
d)
TJ
a
O
•4^
-0
(d
• .H
o
>
Vi
0
•M
v^
a
a
E
c'
3
0
•IH
W
aj
•«->
E
3
u
U
0
^H
U
U
H
V
0)
i;
>
•fl
.t:
■4->
•fH
(D
(0
c b
(3 h
0) lU
V a>
«13
^
(0 4li
(4
1
^
!3
CO
[opes ne
tanding
0)
CO '6
g
C3
o
CO
CO
opei
;tan
•<H
0)
•1H
CO
9)
0
••H
60 ~
&0
1—1 «j
CO
•M
>N
(0
>
M W
•iH
C
c
9> a
1
•ft
1— »
4)
a
0)
•in
•fH
(0
9) 0)
o
0)
0)
0
2
a
w
(0
C/3 3
2
W
(/)
fl
Q
W
H
2
O
U
<
H
Q
2
<
2
O
m
w
ac
H
<
CQ
Q
w
O
a.
I— I
2
O
t-{
H
<
73
CO
D
CQ
H
O
2
2
<
c
E
H
o
•fH
-a
CO
C
o
o
u
E
CD
C
o
CO
>>
60
bO
>,
(U .-
4)
•i-i
in lat
spring
CO
in lat
spring
bo
0-
CO
1—1
C
•1-4
>.
X
4^
1^
CO
■M
a
(0
CO
1
h sap flow
ter early s
CO
■♦J
CO
c
o
•tH
-t-»
9)
•<H
00
rt «
" Jh
^ ^
•»H
u
(U
•i-l
■4-»
l-H
•IH
•IH
E
• iH
»— 1
d
•iH
l-H
CO
CD C
•^ -iH
^
3
'(3
0
0
13
fa
X ^
fa
CO
fa
2
E ^
fa
2
fa
CO
X
1—1
«J
•IH
>
•IH
T3
G
I
09
a
0)
O
G
(0
fl
c:
•c3
•<3
pc:
Pi
u
>
o
o
§
00
o
c
>
o
u
(4
(«
(tf
^
Q
G
1
B
i3
E
a
1
1
o
fH
o
•IH
3
CM ^_^
C4
•13
73
""'s
©"1
"""^
^"^
®
lor
clora
RTU
clora
®
oQ
CM 1
(M 1
O
T3 T3
T3 73
4)
•s
J5 ct
l-H
>
(1)
o§
S§
H "*
H
^
PQ
CQ
PQ
CO
o
>^
l-H
bO
73
O
Pi
o
ca
a
(U
o
CO
c
C (U
a
•IH
•iH S.
•iH
rt
«J 0
«J
ff!
OCj U
Pi
o
l-H
o
I
Ci
o
l-H
u
a
<
CO
1
C
Q
l-H
u
O
I
during the summer or late spring or early fall and are limited by rain
and wind conditions that would result in reduced coverage of the leaves
and movement away from the target plant. When hydraulic sprayers are
used, terrain considerations become important, as the maneuverability of
the machinery is limited in wet areas and in areas of very steep slopes
and large rocks. Basal spraying can be done at any time of the year
except during periods when the lower part of the stem is covered by
deep snow. Based spraying is also limited by rain and snow, which
could wash the material off of the bark during or after application.
Cut stump treatments can also be performed at any time of the year
except for a brief period in late winter or early spring when high sap
flow prevents the translocation of the herbicides into the roots. Like
basal treatment, treatment of cut stumps is not possible during periods
of deep snow cover or when rain or snow would wash the material from
the stump surface.
Table 7 shows that the limitations imposed by weather, season, and
®
terrain vary considerably with individual herbicides. Krenite , for
instance, can be applied only late summer, during the formation of buds
for next year's growth. Other herbicides are limited by their method
®
of application. Tordon RTU (2,4-D and picloram) is used on
rights-of-way as a cut stump treatment, and thus cannot be used
during periods of high sap flow as explained above.
Cost
The following tables present cost estimates of various treatments of
various types of rights-of-way. They can be used as an overall indica-
tion of vegetation control costs, although individual segments of
rights-of-way may differ considerably. The primary factor which
accounts for this variability is the number of stems per acre, or the
degree of stability of the right-of-way. An "out-of-control"
right-of-way may have as much as one stem per square foot while a
stable right-of-way may have only a few stems per acre. While the
out-of-control right-of-way could require use of a large scale rotary
mower followed by an extensive herbicide treatment, the stable
right-of-way may be maintained by one person with a back pack sprayer
101
o o
-4->
O MH
13
o
nS
O
■4-»
U
0)
en
bb 2
u
(0
(0
ni
2
73
o w
(0
C (0
> (0
0) n>
o
(0
C!
O
•4-»
CO
o
73
o •
Si
•4-»
.2 J
•4-»
6Q
<
:3
■«-»
n)
13
00
(0
0)
u
O
I-
O nt
C oo
•i-l CT^
nj .,,_,
<" .
►> t-H
CO
V
u
•IH
>
0)
s **
O cS
U TJ
St-
•»-t OS
■4->
►> (—1
CO
u
• •H
>
u
4)
W
l-H
o
Cnj
O nj
U 13
C CO
O 00
•IH CT\
<» .
CO
u
>
13
u
4>
r an
trie
1„
a> cj
c2
O Ui
cu
0 ctf
CO
C
and
sett
0
CO
O 00
w) 2
u
■tJ rH
C -^x
wS
§
0)
^ «
•«J
Veg
Inc.
^ CO
(0
4) («
0
22
CQ
f
00
W
•J
<
CO
<
(— I
H
w
w
H
en
O
U
CO
6
0
•M
•iH
c
^
E
a
■4-»
o
nt
U
0)
u
H
•IH
VH
•fH
}h
CJ
O
(U
a
w
CO
o
U
^ 0)
o u
u o
nt
0)— .
•— • to
0)
stab
stemi
0)
l-H
J3
I— 1
U3
nt
nt
0)
0)
J5^
•4->
0)
w
oc
w
0)
0)
»H
»4
u
u
V
C3
a>
nt
h
»-,^
u
O
r^
(J
oo
nt
o^
nt
00
"•"^^
1
■-»*.
1
o
o
in
in
o^
o
LO
en
«*
4«-
<«■
■w-
0)
4)
x-s
x-v
}^
>H
0)
V
y
O
»4
h
e nt
@ ni
O
u
l-H --
1—1 ■ —
ni
nt
O
o •
•-««.
I— i ■— !
1—1 ri
•
•
nt
a
@
•— j
@ ^
rdon
ron®
.01 g
rdon
.46 g
0)
•4-»
0)
ni
00
P ^-H
0,-H
h
o
Jho
H fc^ w
H w
U:1
fc^w
0)
u
u
in
? ^
^ CO
V* V
•M
Oj CO
0)
»4
y
(0
-«
(U
V
V
V
o
;^
»^
U
»H
in
y
u
y
y
<NJ
(tf
ni
nt
nt
1
—
"^
--^
o
o
o
t-
r-
vO
t-
>£>
t-
in
l-H
l-H
^f^
■ee-
•€«•
■w-
•€«•
E
■*-»
m
H
a
y
A
y
2
>>
(tf
mh
^
0
«+H
0)
0
a
1
>>
•♦J
•f-t
fn
1=3
4
>>
0)
>
»^
y :i
•Cw
-M
0.0
(Q
0 •
0) u
0)
•t->
••H
a> a
_ w
Sourc
nform
:;a
'rt<
t-t
(0
■M
1
ional
pera
77)
^
•♦-> 0 ryv
0
rtJ 0 ^
Z,
ZUw
u
o
a
0)
Ik
0)
S "
re .fH
S U
o w
(0
rt CO
'So?
a. ^
> (0
2S
o
(0
•iH
o
•4->
o
3
'5 T3 ^ >^
£ 2 § ^
U
^4
o
N
•4-> P
o
fi C rt
O '"H w
••-» rr to
^•^
CO
0)
■H 1— '
U Oh ^ 13
(0
nl
o
Z.
M
u
■*■>
u
•
a;
0
•—J
0
w
(0
(0
13
<
c^
>H
c<-
s
V
0^
D£i
>
1— 1
l-H
>>
C
<o
0)
0
a >
•*-»
0
V4
(TJ
0
3
2 u w
Q
2
n
<
2
0
I— t
U
w
^^
u
00
H
w
w
hJ
0
CQ
U
<
H
(0
C
0
•M
•IH
C!
^
0)
a
c
■M
0
nt
u
0)
^
u
H
•tH
M-l
•IH
»H
U
0
0)
a
w
CO
o
U
O I
■4-»
CO Qi
CO V
u
o
o
u
>
•iH
0)
u
o
(TJ
CO
00
I— I
(Ci
^^
I <u
o b
bO
CO
U 0)
0) CO
l-H
-So
0)
0)
^4
fH
u
u
(«
a
^^
0)
0)
— ^
0
u
»^
0
0
0
0
0
CM
<CJ
a
-^
1
•*-*.^
-**...
1
0
0
in
0
in
0
<M
0
r-i
in
1—1
l-H
^•
-W-
•w-
«-
»4
o
o a>
CO u
fl) "H
!•£
00-^
^ O •*■>
o
■M
)h
>
0)
0)
0
E
4ij
rt
0
>^
in
U
c
nO
4->
(0
■w-
on
O
C
E
H
0)
l-H
u
•IH
73
(U
3
G
1^
a
•iH
0)
0
u
2
00
a
■4->
u
I-H
C!
O I
0) o
•iH
:;3
■4-»
D
Q
2
<
2
O
2
1— 1
U
W
^-^
W
00
H
W
w
J
O
CQ
u
<
H
»H
»4
»4
u
»4
4)
a>
0)
a;
V
•
•M
■*-»
♦J
■«-»
•«->
u
m
(0
(0
CO
CO
<+H 5
c
0)
0)
0)
^
0)
(U
t— 1
u
u
u
•pH
u
o
0 2
»4
u
u
nl
»4
u
'4-'
a>
o
o
o
cai
o
o
a> («
■4->
^
^
^
^
^
V c
■4-»
(0
Sour
nfori
•f-1
•
Q
3
e8
o
•
o
o
e2t
•
o
u
u
•
o
u
■•J
0)
(0
•
o
u
i-<
V 1
•4->
0)
p
§
•iH
73
0
O
u
•
o
iden
oad
^
O
>
>
u
>
^4
^-4
(0
o
>
>-=
•<-»
^
O
u
•S
o
u
5
o
u
•a
(0
CO
CO
0
•;3
g-J3
<
CM pci
CU Pi
CU Cri
S <
cu
Pi
Ou PJ
m
>>
1
o
1
1
0)
•IH ^
'2 E
3
o
o
C 4^
o
+J
O (tf
^
CO
og
u
o
E
0)
4->
oH
^H
•f-«
0)
(Q
:tJ >H
E
I— t
o
o o
a>
u
X
0)
u
•<-»
bO
a
•♦-»
c
•IH
1
1
1
1
1
1
CO
o
o
^
1
1
1
1
1
1
1
CO
o
U
>N
>^
m
(0
^
^
1— 1
1-^
•J3
'53 .
p;
Pi o
0
CO
CO CO
••-»
-<-> CO
4)
CO
CO
=J
3
J3
43
o .
u
ctf O
a
CO O
CO
CO CO
CO
(d CO
(0
2 <
:s
g
(D
0)
p-l
u
l-H
l-H
1
o
4)
1
•«-«
^
9i
(U
o
o
o
t-H
o
o
o
1
E
o
ir>
•1-1
f— (
1
CO
vO
nO
1
1
1— 1
o
-«^
1
o
o
o
o
1
in
o
o
o
o
sO
00
o
o
r~
o
o
CO
(XD
rH
t^
fva
vO
t—i
00
CM
l-H
««^
«3-
•«5-
■w-
<«■
<«■
<«•
<«^
iA^
E
■•-»
(d
0)
H
bO
:3
o
:i
c
o
o
u
a>
•4->
13
•iH
0
u
u
=lH
^
r;
»H
CO
3
<U
»^
fd
2^
§^
8 "
X CO
o
u
■M
o
u
CO
(d
E
ctt
O I
0) o
a >
>^x
•iH
Pi
(0
o
Pi
(0
o 0,
u
(4
u
>
<
1^
o
o
ni
ID
o
00
00
PQ
<
*
O
H
<
U
<
O
w
H
>^
CQ
W
o
<
Pi
H
w
o
U
Q
*-*
U
i-i
PQ
a:
a
o<
c
a
(0
0)
X
E
H
0)
H
bO-M
CM >ji.
o
00
bo
in
^^
O rt
Uo
CO
(U o
o
•
bOo
^0
rt nH
fM
^
■C^
0) ^^
> <u
< oJ
CO
m
sO
o
in
If)
■e/5^
■w-
e
nS
® ^
rt o .i;
Q ^ ^ a
• E
o
C CO
o
HP
<V3
(4
* o
(M -fh
73
Q
I
(d
• IH
ti4
(0
c
C
o
o
''^
l-H
a^
bO
bO
1—1
!h
U
'^
(U
V
•
CL
a
o
o
o
£
in
in
•
•
•^
o
o
0)
<f>
■w-
nJ «J
o
O
3
(fl
(0
^
c
c
-M
o
o
u
1— H
I— 1
<
n]
(d
bO
bO
>>
^
o
in
00
""^
73
VH
t+H
9)
0)
o
•4->
o
4->
U
O
•«->
(0
(0
CU
vw
o
o
0)
0)
u
u
u
l>^
(0
CO
RJ
(d
<u
(U
-4->
;h
TJ
TD
XI
a
3
3
(0
^iH
I— 1
bO
y
CJ
<
E-X3
1— i
3
•<->
^-v <•
"N
D
+j
3
rt JD
W
o
v--- <w
•K-
in
o
TABLE 10
SPECIFIC RIGHTS-OF-WAY OF NEW ENGLAND POWER COMPANY:
COST PER ACRE OF VARIOUS TREATMENTS
Area
Method/
Material
Acres
Cost
Cost /Acre
Fitchburg/
Ashburnham
Krenite®
319 A
$25,100 $78.68
Warwick /Gardner Krenite®
245 A
$19,200 $78.37
Athol
Krenite®
90 A
$ 8,300 $92.22
Erving/
Petersham
Krenite®
375 A $20,924 $55.80
Vernon , Vt . /
Warwick
Krenite®
78 A
$ 6,050 $77.56
Brattleboro/
Bellows Falls
Garlon 3 A®
243 A $14,692 $60.46
No. Reading Hand cutting
10.9 A $ 5,492 $503.85
Mullbury
Tractor mowing 11.4 A $ 3,146 $276.00
Oxford
Tractor mowing 10.5 A $ 1,669 $159.00
Charlton
Tractor mowing 10.6 A $ 890
$84.00
(Herbicide cost includes some handcuttings at streams, gardens, etc.)
106
or chain saw walking the right-of-way, eliminating individual trees.
Another important factor in cost is the amount of clean-up required,
i.e., whether chipping or removal of brush is included in the cost
estimate. Labor intensive clean-up efforts can easily double the cost of
the control treatment.
Some reviewers of the draft GEIR questioned the reliability of the
sources of cost data included in the draft since they were provided by
those who have a vested interest in showing that non-herbicide controls
are unreasonably expensive, i.e., utilities and railroad companies.
These data sources were used because in general they are the only
ones who are generating and recording cost data. One interesting
exception is the data from Citizens for Environmental Protection from
Charleston, West Virginia. Manual control costs from their landowner
demonstration project ranged from $100 to $400/acre compared to $125 to
$657 /acre estimated by utilities and their associations.
Environmental Impact
The impacts of the herbicides covered in this report are addressed in
the literature review presented in Appendix II and in the summaries of
that literature provided in a previous section. The environmental
impacts of physical control methods (excluding fire) include a number of
minor impacts such as increased noise and air pollution from the
machines, and one major impact — the likelihood of causing accidents to
workers. Further comparison of these different types of impact is
presented below in regard to policy evaluation.
107
RECOMMENDATIONS
The information compiled in this report was used to develop policy-
recommendations for the use of herbicides on rights-of-way in
Massachusetts. This policy was developed by a task force that has
been assembled for this purpose. The task force, representing
environmental groups, utility and railroad companies, applicators, local
officials, and various state agencies, among others, generated the
following document.
Introduction
Lately, despite the fact that herbicides are used for many other purposes
as well, public concern has focused on the use of herbicides to maintain
utility and railroad rights-of-way. The use of herbicides on rights-of-way
to control vegetation accounts for approximately 17 to 29 percent of the
total use of herbicides in Massachusetts.
In order to estimate the potential environmental impact of herbicides to
maintain utility and railroad rights-of-way in Massachusetts, the Execu-
tive Office of Environmental Affairs commissioned the preparation of a
Generic Environmental Impact Report on this subject. Preparation of
the Report has been overseen by the MEPA Unit of EOEA with financial
support provided by the Department of Food and Agriculture. The
MEPA Unit also assembled a Task Force representative of the full range
of interests concerned with herbicide use to review the Impact Report
eind to recommend policies the state should pursue with respect to the
control of herbicide use.
The Task Force has considered four general questions in its effort to
translate the findings of the Impact Report into policy recommendations.
These are:
1, Should the state program for regulating the use of herbicides on
rights-of-way be upgraded?
108
2. Should the state establish procedures that will streamline and
coordinate the regulation of herbicide use?
3. Should the state promote the use of "integrated management
techniques" for the control of vegetation along rights-of-way?
4. Should the state classify or group herbicides according to common
characteristics and regulate them accordingly?
In each case, the Task Force considered how such recommendations
would be implemented if the answer were yes. The Task Force answered
the first three questions with a resounding yes. The fourth question
could not be satisfactorily answered at this time. The recommendations
and how they would be implemented are discussed below. The recommenda-
tions should be understood as a whole and implemented in that fashion.
Selective implementation would eliminate the spirit and elements of
compromise which have led to its endorsement by the Task Force.
The six recommendations are:
1. THE EXISTING STATE PROGRAM WHICH REGULATES THE APPLICATION
OF HERBICIDES TO RIGHTS-OF-WAY SHOULD BE SIGNIFICANTLY
ENHANCED.
2. THE STATE SHOULD REQUIRE THE USE OF INTEGRATED MANAGEMENT
TECHNIQUES FOR RIGHT-OF-WAY MAINTENANCE BY REQUIRING
COMPLIANCE WITH APPROVED VEGETATION MANAGEMENT PLANS
BY ALL RIGHT-OF-WAY OWNERS.
3. THE STATE REGULATIONS SHOULD DEFINE GEOGRAPHIC AREAS
OF SPECIAL SENSITIVITY TO HERBICIDE APPLICATIONS AND
RESTRICT SUCH APPLICATION IN THESE AREAS.
4. THE COMMONWEALTH OF MASSACHUSETTS SHOULD COORDINATE
ITS EFFORTS WITH THOSE OF LOCAL GOVERNMENTS TO ESTABLISH
PROCEDURES THAT V/ILL STREAMLINE THE REGULATION OF
109
HERBICIDE APPLICATIONS. THE SUBSTANTIVE AND PROCEDURAL g
REQUIREMENTS FOR OBTAINING AN APPROVED VEGETATION "
MANAGEMENT PLAN SHOULD INTEGRATE THE INTERESTS OF
THE WETLANDS PROTECTION ACT AS THEY PERTAIN TO VEGETATION
MANAGEMENT ON RIGHTS-OF-WAY.
5. THE STATE SHOULD ESTABLISH PROCEDURES WHICH GUARANTEE
AMPLE OPPORTUNITY FOR PUBLIC REVIEW AND COMMENT ON
RIGHT-OF-WAY MAINTENANCE PLANS AND THE REGULATIONS
WHICH GOVERN THEM.
6. REVIEW OF THE CHEMICAL AND OTHER PROPERTIES OF PESTICIDES
SHOULD TAKE PLACE IN THE PESTICIDE REGISTRATION PROCESS
AND IN CONSIDERATION OF VEGETATION MANAGEMENT PLANS.
CLASSIFICATION OF HERBICIDES ACCORDING TO CERTAIN OF
THEIR SIMILARITIES SHOULD BE GIVEN FURTHER CONSIDERATION
BY STATE REGULATORS. HOWEVER, PROMULGATION OF NEW
REGULATIONS FOR CONTROLLING HERBICIDE APPLICATIONS
SHOULD NOT BE DELAYED NOR DEPEND UPON SUCH CLASSIFICATION.'
I
Attachment One lists the members of the Task Force.
Recommendation I
THE EXISTING STATE PROGRAM WHICH REGULATES THE APPLICATION
OF HERBICIDES TO RIGHTS-OF-WAY SHOULD BE SIGNIFICANTLY
ENHANCED.
Discussion
An enhanced state-level program regulating methods used to control
vegetation along utility and railroad rights-of-way is urgently needed.
The quality of current right-of-way maintenance practices varies, even
within existing regulations and guidelines. An effective and reliable ■
110 :
J
state-level program will alleviate the need perceived now by some for
aggressive efforts to regulate these practices at the local government
level. Citizens, local officials, state officials, utilities, railroads,
herbicide applicators, and environmental groups will all most certainly
benefit, albeit in different ways, from a strong, comprehensive state
regulatory program.
The goal of an enhanced, state-level regulatory program should be to
eliminate threats to public health and the environment that might be
caused by herbicide application and, wherever possible, encourage the
use of alternatives to herbicide use. The public's interest in adequate
protection of public health should be accorded consideration equal to
the consideration given to adequate right-of-way maintenance in public
policy decisions. In practiced terms, the program should keep the
application of herbicides to a minimum.
The success of the regulatory program recommended here depends on
the submission of detailed reports on planned activities by utilities and
railroads which must be reviewed, approved, and monitored by technically
qualified personnel at the state level. This workload will require
allocation of additional staff to the state agency (ies) reponsible for
carrying out the program. Given the difficulties of securing additional
staff through the state budget process, attention should be given to
mounting a unified broad-based campaign to secure support for funding
these positions. All interests will be served by capable implementation
of this program. All will be harmed if this is not achieved.
Implementation Steps
1. The goals of the regulatory program should be embodied in statutory
and regulatory language so that the authority to promulgate and
enforce the program is unambiguous and widely recognized.
2. The Department of Food and Agriculture, with the approval of the
Pesticide Board, should promulgate new regulations that keep the
111
application of herbicides to a minimum and encourage the use of
"integrated management techniques". (See Recommendation 2 for
the deteiils of this program.)
3, The Legislature should increase appropriations for at least eight
(8) new positions in the Department of Food and Agriculture to
enable the department to implement the programs called for in
these recommendations. These new positions would provide:
a) capability in environmental analysis to carry out reviews
and approvals of Vegetation Management Plans (2 positions) ;
b) enforcement capability to insure compliance by right-of-way
owners with Vegetation Management Plans (3 positions:
2 inspectors and 1 attorney) ;
c) capability in public information programs to coordinate
public reviews of Vegetation Management Plans (1 position);
and
d) capability in analysis of toxicology and environmental fate
to carry out pesticide product assessments for the Pesticide
Board (2 positions).
4. The Legislature should increase appropriations for at least three
new positions in the Department of Environmental Quality Engineering
to enable the Department to implement the programs called for in
these recommendations. These new positions would provide:
a) for increased hydrogeological capability to identify and
evaluate the extent of areas which contribute water to
public water supplies (1 position);
b) for increased toxicological capability to analyze the charac-
teristics of herbicides (1 position); and
112
c) for increased staff in the Division of Wetlands to review
and approve Vegetation Management Plans for compliance
with the regulations adopted pursuant to the requirements
of the Wetlands Protection Act (1 position). (See Recommen-
dation 4, Steps 3 and 4.)
5, As soon as possible, the Pesticide Board should conduct an in-depth
review of current procedures for registration of pesticides in
Massachusetts. This review should clarify the relationship between
the registration procedures of the U.S. Environmental Protection
Agency as well as the current registration practices of the Board,
identify chemicals which pose unacceptable public health risks,
and, wherever possible, improve current registration practices.
113
Recommendation 2
THE STATE SHOULD REQUIRE THE USE OF INTEGRATED MANAGEMENT
TECHNIQUES FOR RIGHT-OF-WAY MAINTENANCE BY REQUIRING
COMPLIANCE WITH APPROVED VEGETATION MANAGEMENT PLANS BY
ALL RIGHT-OF-WAY OWNERS.
Discussion
The queility of current right-of-way maintenance practices varies, even
within existing laws eind regulations. Therefore the state should require
that all utilities and railroads who maintain rights-of-way submit Vegeta-
tion Management Plans. The Plans should cover the entire right-of-way
system owned and operated by the utility or railroad within Massachu-
setts, document how the goals and regulations of the state program will
be met, and should be kept current. The Plans should provide justifica-
tion for any proposed herbicide use. The Plans should demonstrate
that integrated management practices (i.e. the use of non-herbicide
control practices wherever possible) are being practiced. No applica-
tion of herbicides shoiild be allowed in the absence of a state-approved
Vegetation Management Plan. The requirements of the plan should be
enforceable under provisions of the Massachusetts Pesticides Control
Act.
The obligation to obtain an approved Vegetation Management Plan should
be applicable to all rights-of-way operators, including state agencies
and authorities.
Implementation Steps
1. Vegetation Management Plans should include four parts:
A) Vegetation Management Master Plans
The Master Plan should be filed by each utility and railroad
with the Pesticide Board and DEQE and should describe the
overall approach each one will use to control vegetation along
their right-of-way, including
1) The reasons for managing vegetation.
2) The goal of the plan (e.g. elimination of tree species,
encouragement of low growing plants, vegetation free
areas , etc . ) .
3) The methods of vegetation management proposed and
conditions under which each method would be used.
Type of equipment used for each method.
a) Hand cutting
b) Mechanical cutting
c) Herbicide treatment by type:
- Basal
- Cut surface
- Foliar
- Soil
4) Discussion of the rationale for selection of one manage-
ment method over another.
5) Characteristics of herbicides to be used.
6) Methods for control of herbicide drift.
7) Special treatment strategies for sensitive areas
(See Recommendation 3.)
8) Summary discussion of environmental impacts of management
plan.
9) Average treatment cycle.
10) Persons, and their qualifications, who will develop and
administer the plan.
115
2. The state should examine the application of herbicides to rights-of-way I
not owned or maintained by utilities and railroads (most notably,
those maintained by highway departments) and determine the
extent to which the requirements of this regulatory program should
be applied to all right-of-way owners and operators.
Recommendation 3
THE STATE REGULATIONS SHOULD DEFINE GEOGRAPHIC AREAS OF
SPECIAL SENSITIVITY TO HERBICIDE APPLICATIONS AND RESTRICT
SUCH APPLICATIONS IN THESE AREAS.
Discussion
The regulations should prescribe that these areas be treated in special
ways to minimize any potential harm to public health or the environment
which could be caused by inappropriate herbicide applications. Some of
these areas may be best restricted from any herbicide applications at
all. Some may be restricted to specific methods of application and
specific herbicides.
Implementation Steps
1. The sensitive areas subject to special restrictions ought to include,
though not be limited to, the following:
a) zones of contribution to public water supplies as defined
by the DEQE;
b) private wells and water supplies;
c) shorelines and tributaries of surface public water supplies;
d) areas identified by DEQE as potential future water supplies;
e) open water (lakes and streams) ;
f) gardens and broad-leafed crops in the growing season;
116
g) other crops in growing season, and broad-leafed crops in
dormant season;
h) residential areas, designated parks and recreational areas,
and public gathering places;
i) schools, hospitals, and other structures used by sensitive
populations ;
j) wetlands;
k) critical biological areas (e.g. habitats for rare and endan-
gered species) ;
1) estuaries;
m) wildlife management areas;
n) and other areas designated by the Pesticides Control
Board.
2. In addition to defining these sensitive areas, the regulations
should establish distances within some or all of these sensitive
areas where general applications may not take place. The remainder
of these sensitive areas should be subject to special precautions
established by the Department of Food and Agriculture.
3. Procedures should be established in the regulations to allow for
expansion or contraction of the distances from the center of sensi-
tive areas based upon a petition showing special circumstances or
based upon the development of new scientific information.
4. Within those distances where no herbicide use is otherwise allowed,
some restricted use of herbicides may be edlowed if, and only if,
the owner has demonstrated to the satisfaction of the Department
of Food and Agriculture that no alternative means of control is
available and that there is an overriding public hazard resulting
from the lack of herbicide application. However, this provision
should not be applicable to areas subject to the Wetlands Protection
Act as determined by the DEQE based upon review of Vegetation
Management Plans.
117
Recommendation 4 ^
THE COMMONWEALTH OF MASSACHUSETTS SHOULD COORDINATE ITS
EFFORTS WITH THOSE OF LOCAL GOVERNMENTS TO ESTABLISH
PROCEDURES THAT WILL STREAMLINE THE REGULATION OF HERBICIDE
APPLICATIONS. THE SUBSTANTIVE AND PROCEDURAL REQUIREMENTS
FOR OBTAINING AN APPROVED VEGETATION MANAGEMENT PLAN
SHOULD INTEGRATE THE INTERESTS OF THE WETLANDS PROTECTION
ACT AS THEY PERTAIN TO VEGETATION MANAGEMENT ON RIGHTS-OF-WAY.
Discussion
A cooperative relationship between state agencies and local governments
should be reflected in the design of an enhanced, state regulatory-
program. The state agencies responsible for approval of utility and
railroad plans for control of vegetation along rights-of-way must insure
appropriate opportunity for public comment and review of proposed
pleins, during which time local regulatory and other concerns should be
focused. The objective of these coordinated efforts should be to avoid
duplicative regulation .
The state should encourage cooperative agreements between utilities or
railroads and municipalities and landowners along rights-of-way to
manage vegetation through the use of non-chemical alternatives to
herbicides. The acceptability of these agreements depends in each case
on the resolution of issues deeding with third-party liabilities and
landowner consent, difficult but not unsurmountable problems. It may
not be advisable to implement such agreements for the most heavily
traveled railroad lines.
Implementation Steps
1, The state agencies should integrate the interests and requirements
of all state-level regulatory programs dealing with herbicide applica-
tion on rights-of-way in one approval process.
118
2. The regulations which provide for approval of Vegetation Management
Plans by the Department of Food and Agriculture should be conditioned
on review and approval by the Department of Environmental Quality
Engineering (DEQE) of those portions of the Plans that deal with
wetlands. The DEQE should be required to certify to the DFA
that these portions of the Plans will result in compliance with the
substantive and procedural provisions which protect the interests
of the Wetleinds Protection Act. If the regulations are so drawn,
activities under a Plan approved by DEQE would not constitute an
alteration of wetlands as defined under the Wetland Protection Act
regulations.
3. If possible, the DEQE should establish and publicize criteria for
evaluation of herbicide applications in wetleinds which foster consis-
tency in the review and approval of Vegetation Management Plans.
Such criteria would assist local Conservation Commissions in cases
where they were reviewing a Request for Determination of Applicability
of the Wetlands Protection Act with regard to activities called for
in a Vegetation Management Plan.
4. The state should allow municipal governments and/ or landowners
along rights-of-way to submit proposed alternative, non-chemical
vegetation management plans to utilities and railroads if they
prefer to undertake right-of-way maintenance programs of their
own. These proposals should explain why the proponents believe
their management program is needed. The owner /operator of the
right-of-way should have the burden of showing why such plans
are unacceptable. The Pesticide Board should attempt to resolve
disagreements over the acceptability of an alternative management
proposal in the context of its review of Vegetation Management
Plans .
5. The regulations should encourage the appointment of pesticide
application coordinators at the municipal level and spell out the
responsibilities of such persons. These responsibilities should
include keeping interested citizens aware of proposed and approved
Vegetation Management Plans.
119
Recommendation 5
THE STATE SHOULD ESTABLISH PROCEDURES WHICH GUARANTEE
AMPLE OPPORTUNITY FOR PUBLIC REVIEW AND COMMENT ON
RIGHT-OF-WAY MAINTENANCE PLANS AND THE REGULATIONS WHICH
GOVERN THEM.
Discussion
Recently, citizens of the Commonwealth acting on their own and through
their local governments have expressed considerable concern about the
application of herbicides to rights-of-way. This concern may not abate
simply with the advent of a strong and comprehensive regulatory
program. The state must be sure to provide all appropriate
opportunities for public review and comment as new regulations are
developed and implemented to be sure these concerns continue to be
heard and responded to.
This is especially true with respect to the portion of the regulations
dealing with sensitive areas. The proper designation of the setbacks
from these areas, the way they are defined in general, and their actual
location along particular rights-of-way will be critical to the successful
functioning of the regulatory program. The knowledge and experience
of citizens and local officials will be a valuable addition to efforts to
arrive at proper designations. In particular, the regulatory program
calls for determinations on the acceptability of management practices for
wetlands located in rights-of-way to be elevated from the local level of
Conservations Commissions to the state level as part of the review of
Vegetation Management Plans. This means that local officials must be
assured of notification and opportunity for comment in the review
process for Vegetation Management Plans if the substantial local inter-
ests in wetlands protection available under the Act's procedures are to
be maintained.
120
Implementation Steps
1. Both the regulations and, later, overall Vegetation Management
Plans should be subjected to public review and comment before
being finalized and approved. Copies of the overall plans and
annual notifications should be sent to «ill concerned State agencies
and municipalities.
2. The Department of Food and Agriculture should, at its discretion,
upon request of a state, federal, or local government agency, hold
public information meetings to take comments on proposed Plans.
Before approving a Plan the DFA should demonstrate that concerns
of commenting parties have been addressed wherever possible.
3. The regulations should establish a procedure for appesil by an
aggrieved party of decisions on Vegetation Management Plans.
Recommendation 6
REVIEW OF THE CHEMICAL AND OTHER PROPERTIES OF PESTICIDES
SHOULD TAKE PLACE IN THE PESTICIDE REGISTRATION PROCESS
AND IN CONSIDERATION OF VEGETATION MANAGEMENT PLANS.
CLASSIFICATION OF HERBICIDES ACCORDING TO CERTAIN OF THEIR
SIMILARITIES SHOULD BE GIVEN FURTHER CONSIDERATION BY
STATE REGULATORS. HOWEVER, PROMULGATION OF NEW REGULATIONS
FOR CONTROLLING HERBICIDE APPLICATIONS SHOULD NOT BE
DELAYED NOR DEPEND UPON SUCH CLASSIFICATION.
Discussion
The Task Force has found that the analysis of herbicides to determine
their potential environmental and public health impact is an exceedingly
121
complex process. It requires careful consideration of:
toxicity of the herbicide, (estimated according to avcdlable
toxicological studies) ;
evaluation of the reliability of available scientific data;
mobility of the herbicide in varying soil types (high organic
content soils yield low mobilities);
sensitivity of the area being treated; and
the method of herbicide treatment.
The Task Force gave considerable attention to the possible advantages
and disadvantages of classifying herbicides with similar chemical or
other properties. Some felt such a scheme would allow local officials
and others to understand and comment on Vegetation Management Plans
and the decisions of state regulators on these plans. Others felt such
schemes naturally lead to over-simplified judgements and inappropriate
conclusions because so many important variables cannot be included in
the scheme. In general, the feeling was that educational advantages
would very likely be outweighed by misunderstandings or abuse of such
a scheme.
However, if a method of classification could be developed which was
based on recognized scientific data and analytical methods , it could help
in the review of Vegetation Management Plans. Further consideration of
herbicide classification by the Pesticide Board appears warranted.
Implementation Steps
1. Current registration procedures for testing and/or evaluation of
herbicides should be reviewed and, wherever posr.ible,
strengthened. (See Recommendation 1, Step 5.)
2. Vegetation Management Plans should include a full discussion of the
characteristics of herbicides to be used, including summaries of
relevant and available data on environmental fate and toxicology.
(See Recommendation 2, Step 1.)
121.1
Attachment One
MEPA Herbicides Task Force
Name
Nancy Baker
Jon Beekman
William Benson
Robert Biagi
Ruffin Van Bossuyt, Jr,
Halina Brown
Jeff Carlson
Dennis Coffey
Rita DiGiovanni
Phil DePietro
Beth Ertel
Bill Febiger
Christy Foote-Smith
Carol Greenleaf
Joan Harrison
Elaine Kruger
Genette Maillet
Wayne Melville
Carol Minkwitz
Sam Mygatt
Mary Ann Nelson
Susan Nicker son
David O'Connor
Peter Plansky
John Powell
Mary Richards
John Roy
Roberta Schnoor
Peter Shelley
Robert Stir a
Jeffrey Taylor
Michael Ventresca
Affiliation
MA Executive Office of Environmental Affairs
MEPA Unit
Manager of Water Resources, Cambridge, MA
State Representative, Greenfield, MA
Selectman, Amherst, MA
New England Power Service, Westboro, MA
MA Department of Environmental Quality Engineering
MA Department of Food and Agriculture
MA Railroad Association
MA Executive Office of Transportation & Construction
MA Department of Environmental Quality Engineering
Office of State Senator Olver
Energy Facilities Siting Council
MA Association of Conservation Commissions
Office of State Senator Amick
Harrison Biotech, Cambridge, MA
MA Department of Public Health
Office of State Senator Olver
Franklin County Planning Department, Greenfield, MA
Citizens Pesticide Council, Walpole, MA
MA Executive Office of Environmental Affairs
MEPA Unit
MA Executive Office of Transportation & Construction
Cape Cod Planning and Economic Development Commission
New England Environmental Mediation Center
MA Department of Public Works
Board of Water Commissioners, Holliston, MA
Clinton, MA
Railroad Weed Control, Westfield, MA
Goodwin, Proctor, and Hoar, Boston, MA
Conservation Law Foundation, Boston, MA
Northeast Utilities, Hartford, CT
Vegetation Control Services, Richmond, NH
Associated Industries of Massachusetts, Boston, MA
• 122
0
c
■T
APPENDIX I: SUPPLEMENTAL INFORMATION
c
0
i-i
1-2
CHAPTER 1. LEGAL FRAMEWORK*
This chapter identifies and summarizes applicable federal and state law
affecting the use of herbicides for railroad and electric utility right-
of-way vegetation control in Massachusetts. No attempt is made to
render legal opinions, to resolve apparent conflicts in the law, or to
address issues of policy. Due to space limitations, this chapter should
be viewed as an overview, rather than an exhaustive treatment of the
subject.
Potentially applicable statutes, regulations, and legal doctrines dis-
cussed below include: the Federsil Insecticide, Fungicide and Rodenti-
cide Act and regulations; the Massachusetts Pesticide Control Act and
regulations; the Massachusetts herbicide notification statute; the Pesti-
cide Board's interim guidelines for right-of-way applications; the Massa-
chusetts Wetlands Protection Act eind regulations; the Massachusetts
Clean Water Act; several Massachusetts electric utility and railroad
regulatory statutes; the Federal Railroad Safety Act and regulations;
the Massachusetts Environmental Policy Act; several statutes establish-
ing the regulatory powers of cities and towns with respect to public
health, electric utilities, water supply, zoning and general bylaws; the
Massachusetts Home Rule Amendment; and the doctrine of preemption.
Unresolved legal issues include the scope of the existing statutory
authority of state agencies to regulate herbicide use by railroads and
electric utilities; and whether (and if so to what extent) local regulation
of such herbicide application is preempted by state or federal law.
Description of Applicable Law
A. Pesticide Regulation
1. FIFRA
The Federal Insecticide, Fungicide and Rodenticide Act, as amended by
the Federal Environmental Pesticide Act of 1972 and the Federal Pesti-
cide Act of 1978, 7 U.S.C. §§135-136y (collectively, "FIFRA"), estab-
lishes a establishes a comprehensive federal scheme for the regulation
* primarily by Christopher Davis, Esq., Goodwin, Procter & Hoar
1-3
of pesticides, including herbicides. FIFRA is administered by the
United States Environmental Protection Agency ("EPA"). Among other
things, FIFRA requires, inter alia, the registration and classification
for general or restricted use of all pesticides sold in the United States
(7 U.S.C. §i36a), regulates the labeling of pesticides (7 U.S.C.
§136a) , forbids the use of a pesticide in a manner inconsistent with its
labeling (7 U.S.C. §136(2) (G)), and requires that restricted-use pesti-
cides be applied only by or under the supervision of certified appli-
cators (7 U.S.C. §136b) . FIFRA also establishes a framework within
which EPA may publicly disclose health safety and environmental data
submitted in support of a pesticide registration.
EPA has promulgated detailed regulations implementing FIFRA, 40 CFR
§§162-180. In peirticular, the FIFRA regulations specify the required
contents of pesticide labels, including active ingredients, warnings as
to toxicological and environmental hazards, and applicable use restric-
tions. 40 CFR §162.10. The regulations also specify criteria for the
determination by EPA as to whether a pesticide will cause "unreasonable
adverse effects on the environment," in which case its registration may
be denied or cancelled. 7 U.S.C. §136a-(c) (5)-(6) ; 40 CFR §162.11.
Among the herbicides, EPA has classified only picloram as "restricted
use" on the basis of its hazard to non-target vegetation. 40 CFR
§162.31.
With respect to the trade secret disclosure, the recent United States
Supreme Court decision of Ruckelshaus v. Monsanto Co. , 52 U.S.L.V/.
4886 (June 26, 1984), upheld a provision of FIFRA which relates to
public disclosure of, among other things, data that has been designated
by an applicant for registration as "trade secrets or commercial or
financial information" under another FIFRA section, 7 U.S.C. §136h(b).
The provision had been challenged by a pesticide manufacturer who
argued that the disclosure of trade secrets submitted during the appli-
cation process constitutes a taking of property in violation of the
Fifth Amendment to the United States Constitution. The Supreme Court
reasoned that the manufacturer had notice of FIFRA' s disclosure provi-
sions when it chose to submit data, except for data submitted between
1-4
1972 and 1978 under a previous version of FIFRA guaranteeing confiden-
tiality, and that even as to 1972-1978 data, just compensation could be
obtained from the federal court of claims.
Section 136h(d) enacted in 1978 and enforced by both civil and criminal
penalties under Section 1361, provides as follows:
(d) Limitations -
(1) All information concerning the objectives, methodol-
ogy, results, or significance of any test or experi-
ment performed on or with a registered or previously
registered pesticide . . . and any information concern-
ing the effects of such pesticide on einy organism or
the behavior of such pesticide in the environment
. . . shedl be available for disclosure to the public:
. . . Provided further, That this paragraph does not
authorize the disclosure of any information that -
(A) discloses manufacturing or quality control
processes,
(B) discloses the details of amy methods for
testing, detecting, or measuring the quality of einy
deliberately added inert ingredient of a pesticide, or
(C) discloses the identity or percentage quantity
of any deliberately added inert ingredient of a pesti-
cide,
unless the Administrator has first determined that
disclosure is necessary to protect against any unrea-
sonable risk of injury to health or the environment.
(2) Information concerning production, distribution, sale,
or inventories of a pesticide that is otherwise entitled
to confidential treatment under subsection (b) of this
section [data designated as trade secrets or commer-
cial or fineincial information] may be publicly disclosed
in connection with a public proceeding to determine
whether a pesticide, or any ingredient of a pesticide,
causes unreasonable adverse effects on health or the
environment, if the Administrator determines that
such disclosure is necessary in the public interest.
(3) If the Administrator proposes to disclose information
described in clause (A), (B), or (C) of paragraph
(1) or in paragraph (2) of the subsection, the Admin-
istrator shall notify by certified mail the submitter
of such information of the intent to release such
1-5
information. . . . During such period the data sub-
mitter may institute an action in an appropriate
district court to enjoin or limit the proposed dis-
closure. . . . The court may enjoin disclosure, or
limit the disclosure or the parties to whom disclosure
shall be made. . . .
Under this provision, then, states and qualified members of the public
may gain access to some information offered in support of a FIFRA
registration. Other information will be made available to them if the
Administrator of the EPA determines that health or environmental con-
cerns warrant such disclosure.
State Regulation and Federal Preemption
There is a question as to whether FIFRA, as a federal act, preempts
state pesticide legislation not explicitly authorized by FIFRA (and if so,
to what extent) . The only statutory language pertaining to state
registration of pesticides is contained in section 136v(c)(l) which
authorizes state registration for additional uses of federally registered
pesticides to meet "special local needs". At the same time, FIFRA
expressly contemplates some state regulation of federally registered
pesticides, 7 U.S.C. §136v, and authorizes EPA to delegate to the
states primary enforcement responsibility for pesticide use violations, 7
U.S.C» §136w-l. Courts have reached different conclusions as to the
breadth of the regulatory authority embodied in section 136v(a) of
FIFRA which provides that states may "regulate the sale or use of any
federally registered pesticide or device in the State, but only if and to
the extent the regulation does not permit cuiy sale or use prohibited by
this subchapter." Compare National Agricultursd Chemical Ass'n v.
Romiger, 500 F. Supp. 465 (E.D. Cal. 1980) (FIFRA does not preempt
state's right to require additional data from pesticide manufacturers and
distributors as condition of registration) with Pacific Construction Co.
V. Branch, 428 F. Supp. 727 (D. Guam 1976) (FIFRA preempts state's
authority to promulgate import restrictions) .
It should be noted, however, that even if states do regulate federeil
registered pesticides more strictly than EPA, FIFRA prohibits any state
1-6
from "imposing any requirements for labeling or packaging in addition
to or different from those required [by FIFRA]", 7 U.S.C. §136v.
Thus, any state enacting more stringent use restrictions than EPA faces
significant problems in communicating those restrictions.
The Massachusetts Pesticide Control Act ("MPCA") authorizes the Sub-
committee of the Pesticide Board to register for use in the Common-
wealth pesticides, "including pesticides that are federally registered."
G.L. C.132B § 7. MPCA further provides that the Subcommittee "may
require of applicants for pesticide registrations any information that it
deems necessary to determine whether, or how, the pesticide should be
registered." Id. Regulations promulgated pursuant to MPCA state that
"[t]he Subcommittee may register or refuse to register any pesticide for
distribution, sale or use in the Common weed th" according to the stand-
ards and procedures set forth in 333 C.M.R. section 8.00. Section
8.05. On their face, these statutory provisions and regulations appear
to give the Commonwealth broad authority to establish state registration
standards and procedures beyond those which may be authorized by
FIFRA.
A niimber of legal issues might be raised, however, if the Common-
wealth of Massachusetts were, for example, to revise its pesticide
registration program to require submission of health, safety and envi-
ronmental data as a condition of state registration or re-registration. A
significant factor motivating such concerns is the absence of any trade
secret protection in the MPCA. Without such protection, any data
submitted by ein applicant would be subject to the Massachusetts Public
Records Act, M.G.L. c. 66 § 10, and would have to be made available
to the public upon request. Under Monsanto, the possibility of such
broad disclosure might require applicants to make business judgements
weighing the benefits of registration in Massachusetts against the costs
of their divulging trade secrets.
Among the legal issues that would be presented by a more stringent
state registration program are the following:
1-7
(1) Would such a program be preempted under the
Supremacy Clause by the existing FIFRA regis-
tration process?
(2) Would such a program result in an unconstitu-
tional taking of property? See Monsanto. Is the
Fifth Amendment Taking Clause applicable to a
state as opposed to the federal government?
(3) Would such a program be an unconstitutional
violation of due process rights?
(4) Would such a program violate the Commerce
Clause of Article I of the federal Constitution by
unlawfully restraining interstate commerce?
(5) Even if not unconstitutional, would such a
program violate federal or state trade secret
statutes?
(6) Even if not unconstitutional, would such a
program jeopardize common law trade secret
protection?
The resolution of these issues could depend on the scope and details of
such an expanded state registration program.
2. The Massachusetts Pesticide Control Act
The Massachusetts Pesticide Control Act, M.G.L. c. 132B ("MPCA"),
enacted in 1978, establishes a comprehensive state pesticide regulatory
program closely patterned after the federal program under FIFRA. The
MPCA established the Massachusetts Pesticide Board ("the Boaird")
within the Department of Food and Agriculture, which implements the
Massachusetts pesticide program. G.L. c. 132B, §3. The MPCA pro-
vides for state registration of pesticides (id. , §7) , forbids the dis-
tribution of pesticides not registered with the Board (id. , §6) , forbids
the use of pesticides inconsistent with their labeling or use restrictions
(id. , §6A) , prohibits the use of restricted-use pesticides except by or
under the supervision of certified applicators (id. , §6A) , and provides
for state certification of applicators (id., §10).
The MPCA is implemented by regulations promulgated by the Board, 333
CMR §2.00, et seq. These regulations provide that applicators shall
use pesticides so as to prevent "\inreasonable adverse health effects on
1-8
the non-target environment," that right-of-way applications shall be
conducted "to minimize the extent and duration of foliar brown-out,"
that pesticide applications near or adjacent to public water supplies
"shall be made in such a manner as to minimize the risk of adverse
effects to such water supplies," and that for applications of restricted
or state-limited use pesticides to areas of more than 25 acres, per-
mission must be received from the Board and notice given to the appro-
priate local official. 333 CMR §10.03(19)-(21) . The MPCA regulations
also provide detailed standards for the certification of applicators for
particular categories of uses (e.g. , "right-of-way pest control"). 333
CMR §10.05. Violators of the MPCA or Pesticide Regulations are subject
to civil or criminal penalties. G.L. c. 132B, §14; 333 CMR §10.17. On
July 1, 1980, EPA delegated primary enforcement authority of FIFRA in
Massachusetts to the Board through a federal-state cooperative agree-
ment.
3. The Notification Statute
Chapter 722 of the Acts of 1981, G.L. c. 132B, §6B, requires that any
electric or other "utility company" (which the Board interprets to
include railroads), prior to any application of herbicides to their
rights-of-way, notify the mayor, city manager or board of selectmen,
and the conservation commission, of the town in which the application is
to be done, by registered mail 21 days in advance of the spraying, that
herbicide spraying will be done. The notice is to include the approxi-
mate dates of the application, the type of herbicide, information sup-
plied by the manufacturer (e.g., the label), and identification of the
contractor or utility employee responsible for the application. Herbicide
application must be done within 10 days of the dates included in the
notice. The notification statute is silent on the subject of local reg-
ulation of such herbicide use.
4. Pesticide Board Interim Guidelines
In 1982, the Board promulgated two sets of "interim guidelines" concern-
ing herbicide applications to railroad and utility rights-of-way. There
are the "interim Guidelines Relative to the Use of Herbicides on Ballast
Area of Railroad Layouts in Massachusetts" (revised October 15, 1982),
1-9
and the "Interim Guidelines Relative to the Use of Herbicides to Control
Woody Vegetation on Railroad Layouts and Right-of-Ways in Massachu-
setts" (October 15, 1980). The latter is applicable to electric utility
rights-of-way as well as railroads. Both sets of guidelines are intended
to protect drinking water supplies from herbicide contamination, and
prohibit herbicide application within prescribed distances of public and
private wells, surface water supplies, and tributaries thereof. Both sets
of guidelines also contain "general use guidelines" to minimize herbicide
drift or runoff. The Board intends to promulgate definitive regulations
to replace the interim guidelines on the basis of this statewide Generic
Environmental Impact Report on the control of vegetation on utility
rights-of-way and railroad layouts, if the Board determines that such
regulations are necessary.
B. Wetlands Regulation
1. General Regulatory Scheme
The Massachusetts Wetlands Protection Act, G.L. c. 131, §40 (the
"Act") imposes pre-construction review upon projects affecting wet-
lands. The Act prohibits the removal, filling, dredging, or alteration
of certcdn statutorily defined wetland resource areas ("wetlands")
without first filing a Notice of Intent with the local conservation com-
mission and obtaining from the commission a permit known as an "order
of conditions" regulating the proposed work, so as to protect the
affected wetlands Vedues. Regulatory jurisdiction under the Act
attaches to any activity proposed or undertaken within wetlands subject
to protection under the Act, or within 100 feet of certain such areas
Wetland resource areas protected by the Act include "any bank,
fresh water wetland, coastal wetland, beach dune, flat, marsh,
meadow, or swamp bordering on the ocean or on any estuary,
creek, river, stream, pond, or lake, or any land under said
waters or any land subject to tidal action, coastal storm flowage or
flooding." G.L. c. 131 §40. See 310 CMR §10.02(1) (defining
areas subject to protection). The terms "bogs," "coastal
wetlands," "freshwater wetlands," "swamps," "wet meadows" and
marshes are defined in c. 131, §40 primarily in terms of the types
of vegetation characterizing such areas.
I-IO
(the "buffer zone"), which "will alter" a protected wetland area that is
"significant" to the wetland interests protected by the Act (e.g., public
or private water supply, groundwater supply, or the prevention of
pollution). G.L. c. 131, §40; 310 CMR §10.02(2). Activities outside
the protected wetland areas or buffer zone are subject to regulation
only if and when the activity "actually alters" a protected wetlands
area. Id. A project proponent may file a request for a determination of
applicability of the Act to particular land or work; such a determination
(or a notice of intent) is required for work proposed within the buffer
zone. 310 CMR §10.05(3). If the conservation commission determines
that the proposed work is not within the Act's jurisdiction (i^. , either
that the work is not within a protected area or will not "alter" the
wetlcind in question), the work may proceed unless this negative deter-
mination is appealed and overturned. G.L. c. 131, §40; 310 CMR
§10.05. Otherwise, the commission must issue an order of conditions
regulating the project.
The conservation commission is required to act upon a request for a
determination of applicability within 21 days, and must act upon a
Notice of Intent within 21 days after the close of a public hearing upon
that application by issuing either a negative determination or an order
of conditions. G.L. c. 131, §40; 310 CMR §10.05. The commission's
determination of applicability or order of conditions may be appealed to
the Department of Environmental Quality Engineering ("DEQE") within
10 days of the commission's action. DEQE is required to act upon such
appeals within a prescribed time period by issuing, as applicable, either
a Superseding Determination of Applicability or a Superseding Order of
Conditions. Such superseding orders and determinations by DEQE may
be further appealed within the agency by filing a request for an adju-
dicatory hearing within 10 days of such actions. Id. DEQE's final
decision following such an adjudicatory hearing is subject to review in
the Superior Court if appealed within 30 days of the agency's decision.
G.L. c. 30A, §14.
The Act is implemented by the Massachusetts Wetlands Regulations, 310
CMR §10.00 et seq. , which were comprehensively revised by DEQE in
I-ll
late 1982. The revised regulations became effective April 1, 1983.
These regulations define in detail the resource areas and activities
subject to regulation under the Act; the procedures to be followed by-
project proponents, conservation commissions, and DEQE with respect to
proposed projects affecting wetlands; and include detailed provisions
describing the characteristics, significance, and performance standards
for work in particular types of resource areas for both coastal and
inland wetlands. Violations of the Act may be enjoined by the Massa-
chusetts courts, and are punishable by criminal penalties. G.L. c.
131, §40.
Inland and coastal wetlands may also be protected from " alter [ation] or
pollutfion]" by inland or coasted wetlands restrictions established by
orders of the Department of Environmental Management ("DEM") and
recorded in the appropriate registry of deeds. G.L. c. 131, §40A
(inland wetlands restrictions); G.L. c. 130. §105 (coastal wetlands
restrictions). See 302 CMR §§4.00, 6.00 (DEM wetlands restriction
regulations) .
2. The Utility Exemption
The Act specifically exempts from regulation activities otherwise subject
to the Act's provisions which occur
in the course of maintaining , repairing or replacing, but not
substantially changing or enlarging, an existing and lawfully
located structure or facility used in the service of the public
and used to provide electric, gas, water, telephone, tele-
graph and other telecommunications services. . . .
G.L. c. 131, §40 (first paragraph) (emphasis added). Thus, the main-
tenance of existing electric utility lines is exempt from regulation by
conservation commissions and the DEQE under the Act. It appears that
this exemption is not applicable to the maintenance of the facilities of
railroads which, although regulated as "utilities," are not mentioned in
the statute's list of exempted utility structures or facilities.
DEQE also takes the position, based upon the exemption's reference to
"existing . . . structure [s] or facilit[ies] ," that the exemption is
inapplicable to new or proposed power lines, and that it is thus within
1-12
the jurisdiction of local conservation commissions and DEQE under the
Act to regulate herbicide use on new power lines. See Letter from
William J. St. Hilaire, P.E. (DEQE) to Ronald Boches (New England
Power Company) accompanying DEQE Superseding Order of Conditions
(Amesbury, No. 2-58, September 2, 1982); 310 CMR §10.53(3) (d) .
Also, DEQE interprets the maintenance exemption as limited to "gener-
ally accepted maintenance techniques used by the industry as a whole,"
which apparently includes the application of generally used herbicides
by standard application methods (but not the use of unusually toxic
herbicides). See Memorandum from Carl F. Dierker, DEQE Deputy
General Counsel, to Robert P. Fagan, regarding herbicide applications
by electric utility companies (July 22, 1982).
3 . "Alteration"
The critical question in determing the extent of the regulatory authority
of DEQE and local conservation commissions over railroad and non-
exempt electric utility herbicide applications under the Act is whether
the proposed herbicide use will "alter" any of the wetland resource
areas protected by the Act. The DEQE regulations broadly define
"alter" as "to change the condition of any Area Subject to Protection
Under the Act," including for example "the destruction of vegetation"
or "the changing of . . . [the] physical, biological or chemical char-
acteristics of the receiving water." 310 CMR §10.04. Thus, any
non-exempted application of herbicides in protected wetlands or in the
buffer zone which, through drift, runoff, or otherwise, will have any
discernible effect upon a protected wetland area is subject to regulation
under the Act. Whether alteration will result in a particular case is
essentially a scientific question of fact to be resolved in the first
instance by the conservation commission and, upon appeal, by DEQE.
For example, in the case of the New England Power Company's proposal
to construct new power lines through wetland areas in Amesbury and
Groveland, DEQE concluded that "[t]he application of herbicides in this
case clearly has potential impact on the protected interests of ground-
water quality, protection of public and private water supplies, and
prevention of pollution as set forth in the Act , " and thus imposed
1-13
a number of conditions (substantially incorporating the Pesticide Board's
Interim Guidelines) upon the use of herbicides in maintaining the new
power line. Letter from William J. St. Hilaire, P.E., to Morris Cher-
kofsky, accompanying DEQE Superseding Order of Conditions (Grove-
land, No. 30-22, February 28, 1983), p. 2, Letter from St. Hilaire to
Boches, supra , p. 1. In another case, however, DEQE ruled that
while a railroad's herbicide application within the buffer zone was
subject to the Act, no Notice of Intent was required where DEQE found
that spraying would not alter protected wetlands if done subject to
specified conditions. Letter from Rolcind J. Dupuis (DEQE) to Mass.
Railroad Association (Palmer, Appeal/ Superseding Determination, June
23, 1983). The issue of whether railroad herbicide applications will
alter adjacent wetlands is currently before DEQE in adjudicatory appeals
involving the towns of Clinton and Leverett.
C. Water Supply and Groundwater Regulation
1. DEQE Water Supply Regulation
In addition to its authority to protect wetlands, DEQE has broad statu-
tory authority to prevent the contamination of public water supplies.
DEQE has "general oversight and care of all inleind waters and of all
streams, ponds, and underground waters used by . . . any person in
the commonwealth as sources of ice or water supply and of all springs,
streams, and water courses tributary thereto." G.L. c. Ill, §159.
DEQE has general rulemaking authority to issue regulations and orders
"necessary to prevent pollution and to secure the sanitary protection of
all such waters used as sources of water supply. . ." G.L. c. Ill,
§160, DEQE's orders and regulations are judicially enforceable. Id. ,
§164. Chapter 111 also prohibits the discharge "into any stream or
pond, or upon their bcinks ... or into any feeders of such pond or
stream within 20 miles above the point where such supply is taken" of
any "polluting matter, of such kind and amount as . . . will corrupt or
impair the quality of the water of any pond or stream used as a source
of ice or water supply." Id., §167. DEQE is also authorized to make
rules and regulations "for the sanitary protection" of waters used by
the Metropolitein District Commission ("MDC") for water supply pur-
poses. G.L, c. 92, §17. Chapter 92 declares it unlawful to "corrupt.
1-14
render impure, waste or improperly use" any water supply of any town
within the Metropolitan District. Id., §18. Violations of this provision
are subject to criminal penalties. Id., §22.
Pursuant to these statutory authorities, DEQE has promulgated its
Drinking Water Regulations, 310 CMR §22.00, et seq. , which set water
quality standards and contain numerous prohibitions to protect ground
and surface water supplies from pollution. The DEQE regulations
prohibit the discharge of any substance which in DEQE's opinion is
"poisonous or injurious either to human beings or to animals, . . .
directly into or at any place from which such liquid or substance may
flow or be washed or carried into said source of water supply or tribu-
tary thereto." 310 CMR §22.20(3). This regulation applies to "all land
and water courses used as or tributary to a public [surface] water
system," with certain limited exceptions. Id., §22.20(1). With respect
to groundwater supplies, DEQE may order that the operator of a public
water supply acquire at least 250 feet of land (or 400 feet in the case
of a gravel-packed well) surrounding a source of groundwater used for
drinking water purposes, in order to protect such groundwater supply
from contamination, and DEQE "may order greater distances or permit
lesser distances ... if [DEQE] deems such order or permission neces-
sary or sufficient to protect the public health." Id., DEQE apparently
believes that it has the ancillary authority to restrict or prohibit
activities it deems likely to cause contamination of a groundwater supply
within a prescribed "buffer zone" around wells or other groundwater
sources. See St. HUlaire letter regarding Amesbury wetlands, supra,
p. 2. (citing Drinking Water Regualtions) . The DEQE regulations also
prohibit the discharge of any "polluting liquid or other substance of a
nature poisonous or injurious either to human beings or to animals . . .
into any lake, pond, reservoir, stream, ditch, water course, or other
open waters, the water of which flows directly or ultimately into any
waters" used by MDC for water supply purposes. 310 CMR §24.01,
DEQE has taken the position that the above-quoted provisions of its
Drinking Water Regulations authorize it to impose conditions upon
herbicide use for right-of-way maintenance purposes. See St. Hilaire
letter regarding Amesbury wetlands, supra, p. 2.
1-15
2. The Massachusetts Clean Waters Act
The Massachusetts Clean Waters Act contains two provisions that may
apply to contamination of water resources by herbicides. First, in
cases of "discharge of . . . hazardous material into or proximate to any
waters of the commonwealth" responsible parties are jointly and sever-
ally liable to the commonwealth for investigation and cleanup costs,
eoid/or damages to natural resources. This statute also permits recov-
ery of damages to private property, and imposes criminal penalties for
unlawful discharges. G.L, c. 21, §27(14) (repealed on March 24, 1983
by Chapter 7, Acts of 1983, and replaced by G.L. c. 2 IE, to the same
2
effect). Second, G.L. c. 21, §42 prohibits "the discharge of any
pollutant into waters of the commonwealth" without a permit from DEQE,
and imposes civil and criminal penalties for violations. However, under
recent DEQE regulations effective October 15, 1983, it is unclear
whether runoff from herbicide use on rights-of-way requires a dis-
charge permit. Compare 314 CMR §5.05(9) (discharges to groundwater
from "right-of-way maintenance activities" exempt from permit require-
ment), with 314 CMR §3.05 (no such exemption for discharges to sur-
face water) .
D. Electric Utility Regulation
The Massachusetts Department of Public Utilities ("DPU") is charged
with "the general supervision of all gas and electric companies and shall
make all necessary examination and inquiries and keep itself informed as
to the condition of the respective properties owned by such corporation
and the manner in which they are conducted with reference to the
safety and convenience of the public, and as to their compliance with
the provisions of law, ..." G.L. c. 164, §76. The DPU is given
broad rulemaking authority to establish regulations that it deems
necessary to carry out its statutory duties. Id., § 76C. See
Cambridge Electric Light Co. v. Department of Public Utilities, 363
Mass. 474, 494-95 (1973). It has been held that the DPU has "reason-
ably comprehensive" authority to regulate electric transmission lines.
Chapter 2 IE, popularly known as the Massachusetts Superfund
Act, excludes from its definition of unlawful "releases" of
hazardous material the application of pesticides " consistent with
their labeling." G.L. c. 21E, §2.
1-16
and the safety thereof. Boston Edison Co. v. Sudbury, 356 Mass. 406,
418-20 (1969). No DPU statute was found, however, to specifically
authorize the DPU to regulate herbicide use for right-of-way mciinte-
nance by electric utilities. Nor does any DPU statute address the
subject of vegetation control on utility rights-of-way.
The DPU regulations promulgated pursuant to Chapter 164 include the
"Code for the Installation and Maintenance of Electric Transmission
Lines," 220 CMR §125. These regulations deal with the design and
construction of transmission line structures. No provisions relating to
right-of-way maintenance or vegetation control are included among
them.
The DPU is required to approve any local ordinances or regulations
(pursuant to c. 166, § 25) "affecting the erection, medntenance or
operation of a line for the transmission of electricity." G.L. c. 166,
§27. However, an opinion of the Attorney General on the subject
concluded that local board of health regulations restricting the use of
herbicides on utility rights-of-way were not subject to review eind
approval or disapproval by the DPU pursuant to c. 166, §27. Mass.
Atty. Gen. Op. 82/83-12 (May 11, 1983) at 8. (See Part G, infra) .
E. Railroad Regulation
As with electric utilities, no government regulation squarely addresses
the issue of herbicide use or requires the total eradication of vegetation
along railroad rights-of-way. At the federal level. The Federal Rail-
road Safety Act of 1970, 45 U.S.C. §421, et seq., was enacted "to
promote safety in all areas of railroad operations and to reduce railroad
related accidents and . . . deaths and injuries to persons and to reduce
damages to property caused by accidents involving any carrier of
hazardous materials." 45 U.S.C. §421. The legislative history of this
statute does not indicate that roadbed vegetation was a safety hazard of
Congressional concern. Nonetheless, pursuant to this authority, the
Federal Railroad Administration has promulgated federal track safety
1-17
standards, 49 CFR §213.1, which include the following provision gov-
erning vegetation control:
Vegetation on railroad property which is on or immediately
adjacent to roadbed must be controlled so that it does not —
(a) become a fire hazard to track-carrying structures; (b)
obstruct visibility of railroad signs and signals; (c) interfere
with railroad employees performing normal trackside duties;
(d) prevent proper functioning of signal and communication
lines; or (e) prevent railroad employees from visually
inspecting moving equipment from their normal duty stations.
49 CFR §213.37, These regxilations , however, do not prescribe that
such vegetation be controlled through the use of herbicides or any
other particular technique.
The DPU also has broad regulatory authority over rsdlroads, including
"general supervision and regulation of, and jurisdiction and control
over" railways. G.L. c. 159, §§10, 12; Newton v. Department of Public
Utilities , 339 Mass. 535, 541 (1959). Pursuant to this authority, the
DPU has promulgated "Raibroad Safety Regulations," 220 CMR §150.00,
et seq. , which include regulations concerning track inspection, track
maintenance, and track alterations, but have no provisions concerning
vegetation control or right-of-way maintenance. Another statute, G.L.
c. 160, §23 5A, requires all railroads to "keep the full width of all
[their] locations, to a point 200 feet disteint from the center line on
each side thereof, clear of dead leaves, dead grass, dry brush or other
inflammable material. ..." It is questionable whether this statute was
intended to require the eradication of live vegetation along railroad
rights-of-way, as opposed to the clearing of dead vegetation that has
been killed by herbicides or otherwise. No regulations requiring con-
trol of vegetation have been promulgated under this statute.
F. State Regulation of New Facilities
1. Energy Facility Siting
Pursuant to the Massachusetts Energy Facility Siting Act, G.L. c. 164,
§69G, et seq. , electric companies operating in Massachusetts are
required to obtain approval from the Energy Facilities Siting Council
("Council") for the construction of major new or expanded transmission
facilities (69 kV or more and one mile or more in length) . In approving
1-18
a proposed facility, the Council must determine that it will "provide a
necessary energy supply . . . with a minimum impact on the envi-
ronment at the lowest possible cost." G.L. c. 164, §69H.
Where a utility is precluded from constructing an approved facility by
state or local permit denials or other regulatory obstacles, the Council
may upon application issue a "certificate of environmental impact aind
public need" ("Certificate") with respect to such facility, which in
effect constitutes a general composite permit for the proposed facility.
G.L. c. 164, §69K. The Council is authorized to prescribe and amend
terms and conditions of such a Certificate, including conditions to
mitigate or regxilate environmental impacts. Id., §69(0). Council
Certificates may not override local zoning bylaws in effect before an
electric company files for Council approval of a facility. 980 CMR
§6.02(2)(f).
The Council's regulations, 980 CMR §1,00, et seq. , contain no provi-
sions directly referring to herbicide use. The Council's Administrative
Bulletin 78-2, made peirt of its regulations by action of the Council on
December 1, 1978 (EFSC Rule 64,8[3]) requires that a company, before
it may construct a new transmission line, describe its planned mciinte-
nance practices and provide information concerning surface waters and
water courses, aquifers, springs eind major wells, wetlands, private
on-lot wells, and forest type and vegetation to be cleared. The com-
pany must also prepare an environmental assessment of the effects of
the proposed transmission line, including a comparison with at least one
practiced alternative corridor or route. In a 1981 decision, the Council
approved, subject to certain conditions, the use of herbicides by a
utility on a new transmission line right-of-way in Brewster, Dennis,
and Orleans. In re Commonwealth Electric Company, EFSC No. 79-4B
(April 3, 1981).
2. MEPA
The Massachusetts Environmental Policy Act, G.L. c. 30, §62, et seq. ,
requires the filing of notices of intent known as Environmental Notifi-
cation Forms ("ENF") and the preparation and review of Environmental
1-19
Impact Reports ("EIR") for projects meeting certain thresholds pre-
scribed in the MEPA regulations, 301 CMR §10.00, et seq. Appendix C
to the MEPA regulations, 301 CMR §10.32, lists categorical exclusions
and inclusions for determining whether an ENF must be filed eind an
EIR prepared for a particular project. Generally, these rules require
the filing of an ENF, and where indicated the preparation of an EIR,
for projects having significeint state participation (e.g. , through fund-
ing or sponsorship), size, and/or environmental impact. There is no
general requirement in the MEPA regulations that an ENF or EIR be
filed prior to undertaking a particular application of herbicides for
railroad or utility right-of-way maintenance. In the case of work
xindertaken or funded by a state agency (e.g. , the Executive Office of
Transportation and Construction or the Department of Public Works) ,
"[r] outline maintenance of land, water and vegetation, to insure safety
or suitability for the uses to which it is put, . . . and not effecting
any substantial change in use" is excluded from the requirement of
filing an ENF or EIR, including in particular " [a]pplication of pesticides
or herbicides . . . except where a generic environmental impact report
is required, has been filed or is in preparation." 301 CMR
§10.32(2)(f).
In general, projects underteiken by private parties must file an ENF
(and perhaps an EIR, if required by the Executive Office of Environ-
mental Affairs) if they require einy state agency permits listed in 301
CMR §10.32(3) and exceed specified size thresholds. It appears that no
state permits are per se required for herbicide applications on railroad
and utility rights-of-way. However, where DEQE issues a Superseding
Order of Conditions for the "alteration" of more than one acre subject
to the Wetlands Protection Act or affecting more than 500 feet of "bank"
subject to the Act, an ENF is required. 301 CMR §10.32(3) (b) (1) .
Another wetlands threshold, 301 CMR §10.32(5) (a) (2) , requires the
preparation of both an ENF and an EIR for "any project requiring
alteration of 10 or more acres of land subject to [the Wetlands Protec-
tion Act]." This class of categorically included projects would appear
to be a subset of those subject to the one acre wetlands threshold,
supra, and involves the same type of factual determination as to the
1-20
amount of wetlands to be "altered." Note that these MEPA wetlands
thresholds do nt include acreage within the buffer zone, 310 CMR
§10.07(3). Thus, MEPA may apply to certain herbicide applications that
affect wetland resources.
G. Local Regulation and State Preemption
In response to local concerns about potential adverse effects of herbi-
cides on public health and water supplies, a number of cities and towns
in Massachusetts have adopted measures that directly or indirectly
restrict or prohibit the use of herbicides for right-of-way vegetation
control. These local actions have included orders by local conservation
commissions pursuant to the Wetlands Protection Act, Board of Health
regulations and orders, and various types of zoning or "police power"
bylaws, including groundwater protection bylaws, wetlands protection
bylaws, and outright herbicide bans or restrictions. The validity of
such local enactments, to the extent that they purport to regulate
herbicide use, is the subject of considerable controversy. Railroads
and electric utilities, among others, have taken the position that such
local regulation conflicts with, and is preempted by FIFRA and the
MPCA, and that municipalities are precluded from regulating in this
area. Litigation involving the validity of local Board of Health regu-
lations restricting or prohibiting herbicide use is currently pending .
See Town of Wendell v. Bellotti, C.A. No. 15119 (Franklin Superior
Ct.).
1. Specific Statutory Authorities
A number of Massachusetts statutes give cities and towns the power to
regulate in various areas that potentially affect herbicide application by
electric utilities and railroads. Putting aside the question of pre-
emption, several of these statutory authorities appear broad enough on
their face to authorize local regulation affecting herbicide use. These
include the following:
First, pursuant to the Wetlands Protection Act, G.L. c. 131, §40, local
conservation commissions have the authority to issue orders of con-
ditions which restrict or prohibit activities that will "alter" any
1-21
significant wetland resource area. See Part B, supra; Hamilton v.
Conservation Commission of Orleans, 1981 Mass. App. Adv. Sh. 1521,
1528.
Second, pursuant to G.L. c. Ill, §31, local boards of health have
broad powers to adopt "reasonable health regulations," enforced by-
fines, which regulations must be filed with DEQE. See generally Board
of Health of Woburn v. Sousa, 338 Mass. 547, 551-52 (1959).
Third, with respect to electric utilities, G.L. c. 164, § 75 provides that
"[t]he aldermen or selectmen may regulate, restrict and control all acts
and doings of a[nl [electric company] which may in any manner affect
the health, safety, convenience or property of the inhabitants of their
towns." However, the significance of this broad, relatively old statute
is unclear, since it has been held that more specific, recent utility
regulation statutes supersede c. 164, §75 with respect to their subject
matter. New England LNG Co. v. Fall River, 368 Mass. 259, 265
(1975).
Fourth, G.L. c. 166, §25 authorizes boards of selectmen to "establish
reasonable regulations for the erection and maintenance of all lines
. . . for the transmission of electricity" permitted within their towns.
G.L. c. 166, §27 (emphasis added). Such reg\ilations may not take
effect until approved by the DPU. Id. However, the Attorney General
has rendered an opinion that regulations adopted by local boards of
health, rather than selectmen, to restrict the use of boards of health,
rather than selectmen, to restrict the use of herbicides on utility
rights-of-way, are not subject to approval by the DPU pursuant to c.
166, §27, since these regulations were not adopted pursuant to §25.
Op. Atty. Gen. 82/83-12 (May 11, 1983).
Fifth, pursuant to G.L. c. 40, §§39A-E, towns may acquire (subject to
DEQE approval) lands and waters for water supply purposes, and
anyone who "willfully or wantonly corrupts, pollutes or diverts" any
such waters is subject to sioit by the town for treble damages, as well
as criminal penalties. Id. §39G.
1-22
Sixth, under the Zoning Act, G.L. c. 40 A, §5, cities and towns are
authorized to adopt zoning ordinances, which may "regulate the use of
land ... to the full extent of the independent constitutional powers of
cities and towns to protect the health, safety and general welfare of
their present and future inhabitants." Id., §1A.
Finally, cities and towns are authorized to adopt general "police power"
bylaws (i.e., to protect the public health, safety, welfare, and con-
venience) for einy purpose not inconsistent with the state law. G.L. c.
40, §21; c. 43B, §13. (See discussion of Home Rule, infra). Both
general and zoning bylaws are subject to approval by the Attorney
General before they may take effect. G.L. c. 40, §32; see c. 40 A, §5.
2, Home Rule Powers
The powers of Massachusetts cities and towns to enact local ordinances
and bylaws were fundamentally broadened in 1966 by the adoption of
the Home Rule Amendment, Mass. Const., Art. 89, §6, which allows
municipalities to adopt einy local ordinance or bylaw which is "not
inconsistent with" the Massachusetts Constitution or statutes. See also
the Home Rule Procedures Act, G.L. c. 43 B, §13. By virtue of the
Home Rule Amendment, cities and towns are no longer limited, as they
formerly were, to adopting local legislation only on subjects specifically
authorized by the legislature, pursuant to G.L. c. 40, §21. Thus, the
fundamental inquiry in determining the validity of a local regulation is
not whether it is "inconsistent with" state (or federal) law and thus
preempted. See generally Jerison, Home Rule in Massachusetts, 67
Mass. L. Rev. 51 (1982).
3. The Preemption Doctrine
As just noted, the Home Rule Amendment permits municipalities to
regulate only in ways "not inconsistent with" state law. In areas in
which there is state legislation, local bylaws or ordinances "will be
deemed void if they are inconsistent with any portion of the General
Laws." Beard v. Salisbury, 378 Mass. 435, 440 (1979). The same is
true in the case of any conflict between state or local enactments and
federal law. See e.g. , Florida lime and Avocado Growers v. Paul, 373
1-23
U.S. 132, 146-47 (1963). Thus, state and federal legislation preempts
local legislation in any area in which the two conflict, and the legis-
lature clearly has the power to "restrict local legislative action or
denying municipalities power to act at all." Arlington v. Board of
Conciliation and Arbitration, 370 Mass. 769, 773 (1976).
The leading case on the subject of state preemption is Bloom v. Worces-
ter, 363 Mass. 136 (1973). In explaining the standards for determining
whether a town bylaw is "inconsistent with" state law, the Supreme
Judicial Court in Bloom stated that the test is whether the Legislature
intended to preempt local action on a particular subject, and that "[t]he
legislative intent to preclude local action must be clear." 363 Mass. at
155. Where there is no explicit indication of the legislature's intention
in this respect, however, an intention to preempt local action may be
inferred from factors including the existence of comprehensive legisla-
tion on a subject which effectively occupies the field, and specific
statutory provisions describing what municipalities can and cannot do,
or limiting the manner in which cities and towns may act on the sub-
ject. Id. at 155-56. Where the operation of a local ordinance "will in
any way frustrate the achievement of any statutory purpose," the ordi-
nance is invalid. Id. at 155, 158. Conversely, "[i]f the State legis-
lative purpose can be achieved in the face of a local ordinance or
by-law on the same subject, the local ordinance or by-law is not incon-
sistent with the State legislation, unless the Legislature has expressly
forbidden the adoption of local ordinances and by-laws on the subject."
Id. at 156.
Thus, where an ordinance or bylaw (1) directly conflicts with the
express provisions of a statute, (2) frustrates the purpose of a stat-
ute, or (3) attempts to regulate in an area fully and comprehensively
regulated by state law, it will be held invalid. See e.g. , New England
LNG Co. V. Fall River, 368 Mass. 259, 265-67 (1975) (comprehensive
state regulation of gas companies preempted local ordinance on subject) ;
Del Duca v. Town Administrator of Methuen, 368 Mass. 1, 10-12 (1975)
(comprehensive state legislation, "mandatory in its terms," "describing
in detedl what municipalities can and cannot do," on subject of planning
1-24
boards preempts town bylaw regulating terms of office and powers of
broad); Beard v. Salisbury, 378 Mass. 435, 440-42 (1979) (state earth
removal statute preempts town bylaw prohibiting exportation of sand
and gravel excavated within the town); Rogers v. Provincetown, 1981
Mass. Adv. Sh. 1728 (state statute authorizing operation of mopeds on
any public way preempts town bylaw prohibiting rental of mopeds) . On
the other hand, where the local ordinance is wholly consistent with the
purpose of state legislation on the subject and furthers its purpose, the
local regulation will be upheld even it is more stringent or broad than
the state statute on that subject. See e.g. , Bloom v. Worcester,
supra , 363 Mass. at 159-60, 163 (local human rights commission estab-
lished by city ordinance consistent with purpose of state anti-discrim-
ination legislation); Lovequist v. Conservation Commission of Dennis,
379 Mass. 7 (1979) (local wetlands protection bylaw not inconsistent
with Wetlands Protection Act) .
4. Preemption of Local Herbicide Regulation
There is limited Massachusetts judicial precedent on the issue of
whether local ordinances or bylaws which purport to restrict in various
ways the application of herbicides on railroad and utility rights-of-way
are preempted by FIFRA, the Massachusetts Pesticide Control Act, or
any of the other state statutes discussed above. The Attorney General
has disapproved bylaws adopted by the Town of Wendell which
restricted and imposed conditions upon the use of herbicides in various
ways, on the ground that such local regulations of pesticides were
inconsistent with the MPCA, FIFRA, and the state and federal regula-
tions promulgated piirsuant thereto. Letter from Henry F. O'Connell,
Assistant Attorney General, to Town Clerk of Wendell (November 19,
1980). The vcdidity of this disapproval is now being litigated. Wendell
V. Bellotti, C.A. No. 15119 (Franklin Superior Ct.).
The Attorney General has likewise disapproved similar bylaws variously
regulating the use of herbicides and other pesticides adopted by the
Towns of Ashburnham (1979), Bellingham (1980) and Orleans, Leyden,
Leverett, and Wendell (1981). However, in 1983, the Attorney General
approved a bylaw adopted by the Town of Wayland which prohibits
1-25
applications of pesticides (including herbicides) by private parties
which come into contact with the persons or property of others, unless
advance written permission has been obtcdned. See Letter from Henry
F. O'Connell to Town Clerk of Wayland (February 11, 1983). In the
1983 advisory opinion cited supra, the Attorney General noted that
while local board of health regulations restricting herbicide application
were not subject to DPU approval, such regulations "might be unenforce-
able on other grounds which are beyond the scope of this opinion,"
citing analogous cases in which local regulations of utility activities
were held invalid. Op. Atty. Gen. 82/83-12, at 9, fn. 4 (May 11,
1983). The latter issue was not decided, however.
Decisions in other jurisdictions have held that local regulation of
herbicides is preempted under either FIFRA or state pesticide statutes.
See e.g. , Town of Scilisbury v. New England Power Co. , 437 A. 2d 281
(N.H. 1981); Long Island Pest Control Association v. Town of H\in ting-
ton, 341 N.Y.S.2d 93 (N.Y. Sup. Ct. 1973), aff'd, 351 N.Y.S.2d. 945
(1973). Likewise, the legislative history of amendments to FIFRA and
the regulations pursuant thereto suggest that Congress did not intend
to permit local regulation of pesticides. See, e.g. , S. Rep. No. 838,
92nd Cong., 2d. Sess., reprinted in 1972 U.S. Code Cong. & Ad. News
3993, 4066 J 40 F.R, 11700 (March 12, 1975).
Nevertheless, DEQE appears to have taken the position that local con-
servation commissions can restrict utility and railroad herbicide use
pursuant to their powers under the Wetlands Protection Act where such
herbicide use is likely to "alter" protected wetland resource areas. See
Amesbury and Groveland Superseding Orders of Conditions and accom-
panying DEQE letters, supra (regarding proposed power lines). DEQE
did not, however, consider the preemption issue in these cases. More-
over, the Lovequist case, supra, suggests that municipalities could
restrict herbicide use as part of a comprehensive wetlands or aquifer
protection general or zoning bylaw adopted independently of the Wet-
lands Protection Act. However, the above-cited precedent suggests
that at least certain types of local regulation purporting to restrict or
prohibit the use of herbicides may be preempted by FIFRA and the
1-26
MPCA, even if such bylaws are consistent with the Wetlands Act. In
sum, it is fair to say that the extent and manner in which cities and
towns can regulate herbicide use by railroads and utilities for right-
of-way mainteneince is an unresolved issue.
Unresolved Legal Issues
A. Scope, Interface, and Possible Conflicts Among State Agency
Jurisdiction
In addition to the U.S. EPA's jurisdiction to regulate pesticides under
FIFRA, state agencies including DEQE (under the Wetlands Protection
Act, water supply statutes, and drinking water regulations); the Pesti-
cide Board (under FIFRA, the MPCA, state pesticide regulations and
interim guidelines) ; the DPU (under several railroad and electric utility
regulation statutes and regulations); and the Siting Council (under the
Siting Act and regulations) all have varying degrees of potentially
overlapping regulatory jurisdiction over utility and railroad herbicide
application. What potential conflicts or gaps (e.g. , concerning ground-
water protection) are inherent in the current statutory scheme? Which
authority prevails in the event of a conflict?
B. Authority of Cities and Towns to Regulate
Cities and towns, through their conservation commissions, boards of
health, and by the adoption of general zoning bylaws, have adopted or
have the potential to adopt ordinances, bylaws, regulations, and orders
which purport to restrict or prohibit herbicide applications by railroads
eind utilities in various ways. These local actions may take the form of
general prohibitions on herbicide use, facially neutral regulations which
may have the effect of restricting or prohibiting herbicide use (e.g . ,
wetland or aquifer protection bylaws) , or site-specific restrictions on
herbicide application (e.g. , wetlands orders of conditions) , To what
extent are such local regulations preempted by state or federal law?
Does the form of the local regulation or bylaw matter?
C. Possible Federal Preemption of State Herbicide Regulation
To what extent is Massachusetts constrained by FIFRA or other federal
law in adopting legislation or regulations concerning herbicide use for
1-27
right-of-way maintenance? What types of state regulation, if any,
would be preempted by FIFRA?
1-28
CHAPTER 2. LOCATION OF PUBLIC AND PRIVATE WELLS
Applicators need to know the location of private and public wells that
are adjacent to or within rights-of-way. This section discusses possible
sources of information on the location of these wells.
Private Wells
The majority of private wells have not been mapped by any state or
local agency. . A Massachusetts law, St. 1962 c. 513, requires well
drillers to report the location of drilled wells to the Water Resources
Commission. This law has been in effect for over 20 years but has not
been enforced. Although town-by-town files are currently maintained
in the Department of Environmental Management, very few well drillers
(considerably under 25%) have complied with the law. If it had been
enforced, the compiled data base would have consisted of
. . . the name of the owner of the well, the geographic
location of the well (this shall be given accurately to enable
easy plotting on a U.S. Geological Survey Topographic
(1:25,000 scale) Map), well depth, depth to bedrock or
refusal, casing type, casing size and casing length, well
screen type, well screen length, and well screen depth set,
static water level, method used to test well yield, length of
time (in hours) well pumped, drawdown, well yield, and
drilling logs describing the material penetrated.
Future environmental impact assessments would benefit greatly from
renewed efforts to enforce this law.
Individual towns have historically required information on the location of
wells in the construction of new homes to ensure sufficient distance
between wells and septic systems. Some towns have kept records of
the locations of the wells; others have merely reviewed the site plans
and then filed the permits. Poor record-keeping has been the rule
rather than the exception, however; most of the towns contacted in this
study say that the locations of wells of new homes have been adequately
recorded only in the last two to five years. Information on the wells of
homes built prior to that time is essentially non-existent.
1-29
Individual homeowners must therefore provide the information on private
wells. It has been suggested that applicators conduct a survey of
these homeowners in order to map the wells. This, however, would
involve considerable time and effort on the part of the applicators, who
often do not have the necessary resources. Utility and railroad
companies may be able to conduct such a survey if the owners of
abutting parcels can be identified. These property owners can be
asked to mark the location of their wells on hand-drawn maps or on
maps provided by the uitility or railroad companies.
An alternative way to gather this information would be for the towns to
send requests for the information to individual homeowners. These
mailings would request abutters of rights-of-way to identify themselves
and to mark the location of these wells on maps provided by the town,
or on hand-drawn maps of the homeowners' properties. This
information could then be compiled by the town and forwarded to the
applicator, and /or utility or railroad.
This process would take a considerable time to complete. In the
meantime, it should be supplemented by an approach used in Vermont.
In that state, as well as our own, the utilities and railroads are
required to notify the public of impending herbicide applications. In
Vermont, however, the notification must also contain a request for
landowners to supply information to the utility or rziilroad on the
location of any private well within 100 feet of the right-of-way. The
results have not been encouraging, as suggested by the experience of
the state highway department when notifying the public of herbicide
spraying on highway rights-of-way: only 12 phone calls have been
received in 3 years. This approach should therefore be used only as a
short term supplement to a more thorough systematic mapping by towns.
Public Wells
Information on the location of public wells is relatively easy to obtain.
In Massachusetts, public wells have been mapped by the Department of
Environmental Quality Engineering. These maps can be obtained by
calling the district offices: Central (617-727-0886), Northeast
1-30
(617-935-2160), Southeast (617-727-1440), and Western (413-549-6442).
This information can then be transferred to the maps used by the
applicators .
It is recommended therefore that:
1. Information on public wells in the Commonwealth of
Massachusetts should be obtained from the Department of
Environmental Quality Engineering.
2. Information on private wells should be provided by property
owners and assembled by towns or by utility or railroad
companies.
3. Notifications of impending applications should request
information from landowners on the locations of their wells.
1-31
CHAPTER 3. BIOLOGICAL CONTROL FOR RIGHTS-OF-WAY:
ADDITIONAL DISCUSSION*
The first step to be taken in exploring biological control in any
ecosystem should be to study the ecology of the community. This is
true for two reasons: (1) Biological control strategies are not neces-
sarily as obvious as standard ones, and must sometimes be developed
from a knowledge of the basic biology of the system; and (2) the
ramifications of control strategies must be worked out as completely as
possible before trying them out. There are many cases in the litera-
ture of control attempts that backfired because the behavior of a given
species was ignored or because ecological principles were not
understood (DeBach, 1974).
The most important ecological principle to be considered here is
succession, that refers to the changes over time in species composition
of a community, usually in a somewhat predictable order. In north-
eastern United States forests, this usually refers to sequences of
species which colonize open habitats following disturbances, for example
agricultural fields and pastures left unmanaged, tree blowdowns, and
fires. Roughly, the sequence starts with annuals and grasses, pro-
gresses through perennial herbs to bushes to early successional trees,
leading finally to the climax vegetation, which in must of Massachusetts
is probably oak, white pine, and hemlock (Bromley, 1935).
The rights-of-way problem is to keep forest succession from pro-
gressing. Strategies for achieving this end must be based on an
understanding of the forces driving succession. Current theories of
succession can be divided into two groups. In one group succession is
reasonably directional and, therefore, predictable ... It results from
modification of the physical environment by the community; that is,
succession is community-controlled even though the physical environ-
ment determines the pattern, the rate of change, and often sets limits
*
by David Glaser, Biology Department, Harvard University.
I 32
as to how far development can go . . . It culminates in a stabilized
ecosystem ..." (Odum 1969)
In the other group of theories, it is thought that succession does not
always go in one direction and can be slowed down or stopped along a
successional sequence. According to an alternate explanation of suc-
cession put forth by Drury and Nisbet (1973), "most of the phenomena
of succession can be understood as consequences of differential growth,
differential survival (and perhaps also differential colonizing ability) of
species adapted to growth at different points on environmental gradi-
ents. The appearance of successive replacement of one "community" or
"association" by another results in part from interspecific competition
which permits one group of plants temporarily to suppress more slowly
growing successors ... A comprehensive theory of succession should
be sought at the organismic or cellular level, and not in emergent
properties of communities."
Frank Egler (1954a), who has done a large amount of work on
rights-of-way management, termed the first group of theories "relay
floristics," in which each successional stage prepares the way for the
next. He suggested that operating concomitantly with this is a second
factor, the "initial floristic composition." According to this hypothesis,
all or almost all of the species are present when succession starts or
invade very early on, and "development unfolds from this initial flora,
without additional increments by further invasion" (Egler, 1954a)
The three views of succession described above lead to three ideas on
control. By the first view, any attempts at keeping trees out of a
naturally forested ecosystem must always fight an inexorable process.
Trees will always attempt to invade grasses, herbs, or bushes, and so
constant surveillance and periodic treatments to kill tree seedlings are
necessary. The second view, that of Drury and Nisbet (1973), sug-
gests the possibility that, with a knowledge of the biology of individual
species, it may be possible to manipulate natural ecosystems "off the
main track" of succession. Third, a restatement of the theory of initial
floristic composition is that one important factor in succession is
1-3:
"getting there first." Plants have a higher chance of succeeding if
they have advance reproduction. For example, tree species with
seedlings which can remain in the under story of a forest will have a
higher chance of moving into the canopy when a large tree falls than
tree species which cannot tolerate shade as seedlings. By this view,
selectively destroying the appropriate tree species early in succession
may lead to a relatively stable community which is resistant to tree
invasion.
Thus, based on an understanding of the ecology of forest succession,
biological control for rights-of-way is different from other biological
control situations. The goal in most cases is to limit or eradicate a
given species from a given type of environment; for example, to reduce
the populations of gypsy moth in forests of the northeastern United
States. This is usually accomplished by adding to the ecosystem an
antagonistic species; for example, the nucleopolyhedrosis virus for
control of gypsy moth. However, adding a non-native species to a
right-of-way is extremely dangerous, because of the possibility that the
controlling agent will affect the forest outside the right-of-way. Here,
the problem is to create a specific pattern of distribution among
existing species, and in most cases this means keeping a thin strip of
land through forest (or what would become forest if left alone) in an
early successional state. Instead of trying simply to reduce the density
of target species, it is more useful to approach the problem as one of
establishing a community of competitors that can keep trees from
invading .
Mechanism of tree inhibition by shrub and herbaceous communities
The next step is to explore the possible mechanisms by which treeless
plant communities could exclude trees. In this section, proposed
mechanisms are reviewed. In the next, examples of communities stable
to tree invasion are given.
Several mechanisms have been proposed to explain how dense shrub,
grass, forb, or fern communities can prevent or reduce tree seedling
growth. No case is fully understood. Competition for light, nutrients.
1-3^
and moisture is probably important to some degree in all or most cases
(Niering and Goodwin, 1974), At least in some cases, the desired
species are able to outcompete tree seedlings if they are given a head
start. There are three ways in which plants can invade open areas
quickly. Plants such as ferns and some weeds have seeds that are
numerous, tiny, and wind-dispersed. Another mechanism is vegetative
spreading, that is, without seeds. Bramble and Byrnes (1982) found
that most of the species in their stable communities spread by sending
up shoots from rhizomes, underground stems that run horizontally.
Once a single plant is established from seed it can spread to cover an
area with dense growth which may outcompete any other seedlings
within its borders.
The third way to get a head start is to have shade-tolerant seedlings in
the forest understory, which can enter the canopy as soon as a space
is made available, Horsely and Marquis (1983) described studies of
Grisez and Peace (1973), in which the presence of advance reproduction
was found to be the most important factor determining whether forest
regeneration occurred on clear-cut Pennsylvania lands.
Soil conditions are extremely important determinants of the success of
plant species, Horsley (1977a) describes clear-cut areas in
Pennsylvania that failed to regenerate, due at least in large part to
fires which destroyed much of the organic matter of the soil and to
poor drainage along stream bottoms or in high flats underlain by
fragipans, (hard, impermeable underground layers). Niering and
Goodwin (1974) suggested that heaths, (communities of ericaceous
shrubs such as blueberry and huckleberry) may inhibit tree establish-
ment by buildup of acid duff. Also, preliminary data of Warren and
Niering (1973), as reported by Niering and Goodwin (1974), suggest
that moisture stress under huckleberry clones may be important.
Bramble and Byrnes (1982) in their study of a Pennsylvania right-of-
way, concluded that "while it appears that there are cases where cer-
tain shrub communities are relatively permanent and highly resistant to
tree invasion, these usually occur under special conditions of habitat
1-35
such as sites highly unfavorable for trees, or where human and animal
disturbance and fire are continuous."
Grazing can affect species composition of plant communities. Horsley
and Marquis (1983) concluded that deer browsing affected growth of
certain species of trees as well as blackberry and raspberry in
clear-cut areas of central Pennsylvania. Little bluestem grass
(Andropogon scoparius) , which may be stable to tree invasion (Niering
and Goodwin, 1974), is destroyed by grazing (Bromley, 1935).
Fire is also an important determinant of species composition. Many
species that are desirable for right-of-ways, such a little bluestem, are
common invaders of burned-over areas (Swan, 1970; see also chart
below) .
Finally, allelopathy has been implicated in resistance to tree estab-
lishment (Horsley, 1977a and b). Allelopathy is the production by a
plant of chemicals inhibitory to another, Horsley studied the failure of
certain areas in Pennsylvania to reforest following clear- cutting. He
found that washings from goldenrods, asters, and ferns inhibited seed
germination and seedling growth of black cherry.
In summary, many mechanisms have been considered to account for the
inhibition of tree establishment by certain plant communities. Some
factors, such as soil type, are likely to be of some importance in all
cases. Other factors, such as allelopathy, have been implicated by
experimental evidence in specific cases. At this point, it is impossible
to describe definitively and completely the mechanisms of inhibition in
any given case.
Examples of Plant Communities Stable to Tree Invasion
The next question to be asked is: Are there plant communities where
competitors that resist tree invasion have been established, either
purposefully or fortuitously? The answer for the northeastern United
States is yes, both purposefully and fortuitously.
1-36
There are several examples of plant communities established by various
types of environmental perturbations, that simply are not invaded by
trees. Niering and Egler (1955) reported a stand of Viburnum lentago
in southwestern Connecticut, considered to have arisen fortuitously on
an old pasture, which had no tree invasion for at least 25 years,
Niering and Goodwin (1974) mentioned communities of witch hazel,
speckled alder, sheep laurel and other species in various parts of
Connecticut which appeared stable to tree invasion for up to several
decades.
Foresters have long noted that certain shrubs, herbs and grasses can
inhibit forest regeneration. Their problem is a potential boon for
rights-of-way management. For example, Horsley (1977a and b) de-
scribed areas in northwestern Pennsylvania, clear-cut and burned fifty
years previously, which stiU had no or little tree regeneration. These
areas had dense ground cover dominated by grasses, goldenrod, aster,
and ferns. In the southeastern United States, forest regeneration on
some three million acres of land has been prevented by thickets of
rhododendron and mountain laurel (Wahlenberg and Doolittle, 1950,
McGee and Smith, 1967).
There are also examples of rights-of-way, under various management
schemes, on which communities stable to tree invasion for up to several
decades have been established. Niering and Goodwin (1974) selectively
sprayed a power line right-of-way in Connecticut in 1953; periodically
they re-treated the area to root-kill small amounts of new reproduction
and trees initially missed. In 1970, the line was reconstructed and
trees within the right-of-way were given a basal treatment. These
treatments resulted in a mosaic of relatively stable shrub communities
and less stable herblands. Areas of continuous dense shrub cover
resisted tree establishment for at least 15 years. The major shrub
species involved were smooth alder, coast pepperbush, winged sumac,
northern arrowwood, blackberry, greenbrier, and hay scented fern.
Very little invasion occurred in clones of blueberry (Vaccinium
vacillans) , huckleberry, and greenbrier. In addition, pure stands of
little bluestem grass showed remarkable stability. The authors
1-37
recommended that "in view of the stability of shrub communities and of
the possibility of encouraging them through the selective removal of
tree growth, the potential for creating shrub cover in vegetation
management is great."
Bramble and Byrnes tested various tree-removal methods on a power
line right-of-way in Pennsylvania. The line had been cleared in
1951-52 and was sprayed in 1953. Follow-up basal treatments were
given in 1954 and 1966. Spot cutting and stump spraying were carried
out in 1978-79 to control the tallest trees. In 1980 and 1982 selective
basal spray was applied. They found that a dominant shrub cover
interspersed with herbaceous openings developed on all treatment areas
over 30 years. Some of the major species were the same as those found
by Niering and Goodwin (1974).
However, in contrast to Niering and Goodwin (1974) , Bramble and
Byrnes (1976) stressed that some shrub species were resistant to tree
invasion and others were not; that is, the life form (for example, shrub
vs. herb vs. grass) was not as important as the particular species
involved. They found that the patches with fewest invading trees in
1976 had low early blueberry, bear oak, meadow fescue, and mixtures
dominated by fescue and narrow leaved goldenrod. The patches with
the heaviest tree seedling densities were huckleberry, rough goldenrod
and blackberry, as well as mixtures dominated by rough goldenrod,
hay scented fern, sweet fern, and blackberry. The dominant community
type throughout the thirty years was composed primarily of bracken
fern, sedge, loosestrife, and blueberry; in 1976 this community covered
27% of the right-of-way and had the second highest density of trees
emerging above the group cover.
Bramble and Byrnes (1982) concluded that "areas that remained
absolutely stable on the right-of-way over the thirty years were rare
indeed" . It appeared that what seemed to be stable communities were
in fact mosaics of cyclic changes operating at the local level. There
was a constant trend of the fern, grass, herb, and shrub vegetation
towards development of a dominant shrub cover.
1-38
(
In 1934-36 a fire line was cleared and harrowed through a southeastern
New York forest. Most of the line developed a brush community,
including trees. One part produced a complex of stable treeless
communities which until at least 1953 resisted tree invasion (Pound and
Egler, 1953). The communities included ferns, sedge, and bushes.
Horsley (personal communication; September 8, 1983) described a power
line right-of-way in Pennsylvania that had been sprayed once 40 years
ago and on which a community of ferns developed. Tree seedlings did
germinate in the community, but the seedlings did not emerge above the
fern cover.
One must be extremely careful when comparing plant community
dynamics of different regions, because of differences in temperature,
rainfall, soil types, and species composition. None of the above cases
is in Massachusetts. However, most of the important species mentioned
in the studies do occur in Massachusetts. Species that are problematic
in other regions may not be so in Massachusetts. Also, the resistances
of plant species to tree invasion may change at different latitudes.
The set of forces driving community dynamics are likely to be the same
throughout the northeastern United States, although the relative
importances of them will vary region to region. By studying cases in
different regions, one can learn under what conditions what forces are
important and use this information to extrapolate to the region of inter-
est.
In summary, several examples of arrested or retarded succession are
known in the northeastern United States. The communities arise in
these areas either fortuitously, through selective herbicide use and
mechanical control, or following logging and burning. Several species
are found in more than one community. There are no absolutely stable
communities, only some communities with relatively greater stability than
others. Although Niering and Goodwin stress the stability of shrub
clones, they, along with Bramble and Byrnes, also stress the concept
of relative stability, as opposed to the idea of climax in classical
1-39
succession theory. In addition, life form is not a sufficient indication
of resistance to tree invasion. The particular species involved must be
considered.
Species associated with the inhibition of tree invasion The following
provides a brief description of a few of the species that were found to
be components of stable communities that resisted tree invasion over
time.
An drop og an scoparius (little bluestem) is a grass that can tolerate
a variety of conditions, including open woods, pinelands, dry clearings,
prairies, and open rocky areas on hilltops. It forms a deep root sys-
tem that can limit the invasion of all trees except those that have a
deep initial taproot. The dense, fibrous root system successfully com-
petes with trees for moisture, particularly at lower soil depths.
Andropogan often dominates old fields and can form a thick cover,
particularly if burned (Bromley, 1935; Jorgensen, 1978; Richards,
1973).
Dennstaedtia punctilobula (hay-scented fern) is a fern that will
grow in a rocky or low-nutrient soils in wet or dry conditions. It can
form dense colonies in pastures and roadsides. It was found to inhibit
tree invasion in an Allegheny Plateau forest in Pennsylvania after trees
were cut (Cody et al. , 1977; Horsley, 1977b).
Gaylussacia baccata (huckleberry) is a shrub that grows in a
variety of conditions such as dry or moist woods, thickets, clearings,
and swamps. It is favored by fire and can be cultivated by seed. On
a right-of-way in Connecticut, it was found to be a part of a stable
shrub community, forming dense clones. It was also part of a
right-of-way community where it was found to be one of the species
most resistant to tree invasion (Fernald, 1950; Petrides, 1972; Niering
and Goodwin, 1974; Egler, 1954b).
Hamamelis virginiana (witch hazel) is a shrub found in dry or
moist woods. It can persist for many years by means of basal suckers.
1-40
but expansion requires reseeding. In East Haddam, Connecticut, it was
present as thickets in abandoned pastures which were found to be
stable for 40 years. It has also been found in stable shrub communities
in southeastern New York and on a right-of-way in Connecticut. On a
central Pennsylvania right-of-way, it was found to be sparse but
consistently present, forming a shrub border at the forest edge
(Niering and Goodwin, 1974; Bramble and Byrnes, 1972; Pound and
Egler, 1953; DeSteven, 1982).
Kalmia angustifolia (sheep laurel) is a shrub found in old pas-
tures, rocky hilltops, barrens, bogs, open woods and in wet or dry
soils. It is often found in areas with a history of forest fire. In
spruce-fir forests of Newfoundland, it has been found to form a domi-
nant cover after fires, resisting tree invasion almost indefinitely. It
may also be allelopathic, since a water-soluble extract has been found
to inhibit root growth of black spruce. In Marlborough, Connecticut,
pure clones have been found to be stable to tree invasion for several
decades (Jorgensen, 1978; Niering and Goodwin, 1974; Fisher, 1977).
Pteridium aquilinum (bracken fern) is tolerant of both shade and
full sun, and can grow in infertile, sandy, and acidic soils, as well as
in woods, old pastures, and burned-over areas. Among foresters, it is
considered to have the ability to inhibit reforestation, and has been
found on several rights-of-way that are stable to tree invasion (in
Connecticut, New York, and Pennsylvania). It is considered
allelopathic to black cherry and a number of other trees. (Horsley,
1977a; Richards, 1973; Pound and Egler, 1953; Neiring and Goodwin,
1974; Bramble and Byrnes, 1972).
Solidago spp. (goldenrods) are herbaceous plants that are com-
monly found throughout much of Massachusetts in clearings, along
roadsides, and on the borders of woods and streams. Several studies
have indicated that it may be allelopathic to trees, including black
cherry, yellow poplar, and sugar maple. It responds well to cultivation
and can be encouraged by the addition of nutrients (Horsley, 1977a;
Richards, 1973; Fisher et al. , 1978; Goode, 1980).
I-il-l
Vaccinium spp. (blueberry). In Massachusetts, blueberry grows
in poor acid soils of pastures, in rocky areas, swamps, under oak
canopies, and other habitats. Low blueberry has been found in stable
shrub communities in Connecticut and Pennsylvania. In Pachaug State
Forest in Connecticut, attempts to reforest large tracts of land have
been thwarted by high densities of blueberry. The only regular care
given most blueberry fields is burning every 2 or 3 years, although
fertilization promotes their growth (Thomson, 1977; Niering and
Goodwin, 1974; Bramble and Byrnes, 1976).
Rub us allegheniensis (blackberry) is a shrub found in dry
clearings and thickets, although it grows best in moist, rich soil in
open woodlands, and along fences and roadsides. It is a component of
stable vegetative communities in Connecticut, southeastern New York,
and central Pennsylvania. It has been recommended as an appropriate
crop for rights-of-way (Niering and Goodwin, 1974; Bramble and
Byrnes, 1976; Duncan, 1935; Goodland, 1973; Pound and Egler, 1953).
1-42
TABLE I-l
SPECIES IMPLICATED IN INHIBITION OF TREE ESTABLISHMENT
Common name
Scientific name
Bushes
Alder , smooth
Alder, speckled
Arrowwood
Blackberry
Blueberry, late low
Blueberry, early low
Blueberry, highbush
Dogwood, gray
Greenbrier
Hazelnut
Honeysuckle , Japanese
Huckleberry
Juniper , common
Loosestrife
Meadowsweet
Mountain laurel
Nannyberry
Pepperbush, coast
Sarsaparilla, wild
Scrub oak
Sheep laurel
Sumac, winged
Sweet fern
Teaberry
Witch Hazel
Alnus serrulata
Alnus rugosa
Viburnum recognitum
Rub us allegheniensis
Vaccinium angustifolium
Vaccinium vacillans
Vaccinium corymbosum
Cornus racemosa
Smilax rotundiflora
Corylus spp.
Lonicera japonica
Gaylussacia baccata
Juniperus communis
Lysimachia quadrifolia
Spiraea latifloia
Kalmia latifolia
Viburnum lentago
Clethra alnifolia
Aralia nudicaulis
Quercus ilicifolia
Kalmia angustifolia
Rhus copallina
Comptonia peregrina
Gaultheria procumbens
Hamamelis virginiana
Ferns
Bracken fern
Hay-scented fern
New York fern
Pteridium aquilinum
Dennstaedtia punctilobula
Thelypteris (Dryopteris)
noveboracensis
Grasses
Little bluestem grass
Fescue, red
Grass
Grass, short husk
Panic grasses
Sedge, swamp
Andropogon scoparius
Festuca rubra
Calamagrostis cinnoides
Brachyelytrum erectum
Panicum spp.
Scirpus cyperinus
1-43
Sedge
Sedge, vernal
Upland rice grass
Carex crinita
Carex pensylvanica
Oryzopsis asperifolia
i
Forbs
Aster
Fireweed
Flat pea
Goldenrod, Canadian
Goldenrod, grass-leaved
Goldenrod , wrinkled
Aster spp.
Erechtites hieracifolia
Lathyrus sylvestris
Solidago canadensis
Solidago graminifolia
Solidago rugosa
I'U-k
CHAPTER 4. A METHOD FOR MARKING RIGHTS-OF-WAY
A method is needed for marking areas that should not be sprayed on
rights-of-way. Zones around wells or wetlands, for example, need to
be identifiable to an applicator. The most reliable way to mark areas
not to be sprayed is by identifying them on maps carried by the
applicator as he moves along the right-of-way. Maps are more reliable
than physical markers, which can deteriorate or be vandalized or
obscured by vegetation. Physical markers on the rights-of-way should
supplement the use of a map. Particularly sensitive points such as
wells located within rights-of-way should be marked with a painted
metal stake or a wooden stake treated to retard degradation.
Additionally, "Warning" markers should be placed on the rights-of-way
to give advance notice to an applicator that the segment he is
approaching contains an area that should not be sprayed. Advance
warning is particularly important on railroad rights-of-way, where the
vehicle applying the herbicide may approach a sensitive area suddenly.
A simple system to provide this advance warning would be to use
colored signs that would tell the applicator when he was approaching or
leaving a sensitive segment. On a utility rights-of-way, these signs
(possibly colored metal plates) could be placed on transmission line
structures. Different colors would indicate "approaching" or "leaving"
a sensitive segment. Each structure that bordered a sensitive area
would have two signs, one of each color on each side, so that the
segment could be approached in either direction.
On railroad rights-of-way, the same system would be used with the
signs attached to the poles running along side the tracks which carry
the communication lines. The signs would be placed a short distance
away on either side of an area not to be sprayed (e.g. 100 feet).
Again there would be a rule for colors indicationg entering and leaving
the segment, and again two signs of different colors would be on each
pole marking the edge of the segment.
1-^5
Further consideration of these problems are needed by structural eng- ■
ineers and others able to design a system that is easily maintained over
long periods and that does not interfere with railroad or utility
right-of-way function or safety.
(
(
1-^4^6
CHAPTER 5. SPILL CLEANUP
The following information is intended to provide examples of ways to
minimize adverse effects of pesticide spills and the disposal of unused
material and pesticide containers. This discussion is not meant to
provide adequate information to those responsible for reacting to a spill
of pesticide material. Additional information can be obtained from the
Pesticide Board of the Massachusetts Department of Food and
Agriculture.
Spill Cleanup
Before a spill occurs, a contingency plan should be prepared and a
clean-up kit should be assembled. Applicators should be familiar with
the contingency plan, which should include specific procedures to be
followed for liquid and dry herbicides, phone numbers for emergency
services, and names of persons to be notified. Spill kits should include
copies of the contingency plan, along with such items as a 5-gallon
drum, protective clothing, a large quantity of absorbant material (such
as sawdust, a floor- sweeping compound or vermiculite) , a tarp for
covering the spill, first aid materieil, a shovel, and plastic bags.
When a spill occurs, after any injuries have been attended to, the fol-
lowing stops should be taken:
1. Liquids should be prevented from spreading by trenching or
diking the area with absorbant material or inert materials such as
sand.
2. The spill should be covered. If it is dry, a tarp can be placed
over it or a light sprinkling of water can be applied. Liquids
should be covered with absorbant material.
3. Dry spills should be removed by sweeping up small areas at a
time, gradually unrolling the tarp to uncover areas to be swept.
For liquid spills, the absorbant should be worked into the spill to
assure that it thoroughly soaks up the liquid.
1-^7
4. Dry material or the absorbed liquid should be placed in heavy
duty plastic bags or other leakproof containers and labeled.
5. The soil under the spill should be dug to a depth of at least three
inches below the depth to which the liquid penetrated. Contam-
inated soil should be placed in leakproof drums and labeled.
6. All material should be disposed of in an approved hazardous waste
disposal facility.
Specific information on spill cleanup for individual herbicides can often
be obtained from the material safety data sheet provided by the man-
ufacturer. For instance, the recommendations for spill clean up provid-
®
ed by Dow Chemical U.S.A. for Garlon 4 are as follows: "Dike large
spills. Keep out of streams and domestic water supplies. Absorb small
spills in inert materials such as sand." Recommendations for diquat by
Chevron Chemical Company include directions to scrub the area using a
detergent, after picking up the material with absorbants such as clay
or loam soil.
Unused pesticide materials should be placed in leakproof containers,
labeled, and transported by a licensed hauler to an approved hazardous
waste disposal area. Unused pesticide material should not be flushed
down drains. Glass, metal or plastic containers should be triple
rinsed, crushed and placed in a waste storage drum, and taken to a
local landfill. No pesticide container should ever be reused for any
purpose, even after thorough washing. Additional information on
container disposal can sometimes be found on the label, although some
labels, directions, may not be recommended in Massachusetts (e.g., the
Aminotriazole Weedkiller 90 label recommends that bags be burned) .
Individuals should be consult the Massachusetts Pesticide Board for
final recommendations. Additional detail is given in a document by the
Armed Forces Pest Management Board (1980), from which much of this
information was obtained.
1-48
CHAPTER 6. SOILS IN MASSACHUSETTS*
The following discussion presents some rough generalizations concerning
the physical characteristics and terrain of 4 areas in the Commonwealth.
The generalizations were obtained from a review of the Soil
Conservation Service data sheets regarding the locations and
descriptions of individual soils.
Western Massachusetts
In this area, typical soils are fine sandy loams (in which fine sand,
0.02 to 0.2 mm, is dominant) which frequently are overlain by thin
organic matter. Bedrock outcroppings are common in these "rugged"
areas, and depth to bedrock is often very shallow (less than 20
inches) .
Slopes are as high as 50%-80%. The soils in this area are often
well-drained (2.0 to 6.0 inches per hour) and often quite acidic (pH as
low as 3.6). Lateral movement of water is likely where the bedrock is
near the surface. Runoff can be expected to be rapid in areas of
frequent bedrock outcropping
In areas where the depth to bedrock is greater, fine sandy loams are
often underlain by compact glacial till. Frequently a fragipan, a dense-
ly compacted layer of soil, is found one to three feet below the surface.
Above the fragipan, the soil is moderately permeable (0.6 to 6 in/hr) ,
but once it reaches the fragipan it is slowed (to as a little as 0.06
in/hr) , resulting in a tendency for the water to move laterally.
Compared to the soils underlain by bedrock, these soils are less acidic
(4.5 to 6.0) and rugged (slopes of 0 to 35%).
Central Massachusetts and Middlesex County
A variety of soil types exist in the area extending from the Connecticut
River Valley to the coast although these soils are somewhat evenly
♦Information from Arthur D. Little, Inc. (1979)
I-'^9
distributed through this area. The main soil types found in the
Boston area, for instance, ate the same ones found near Worcester.
Some of the soils in this area are similar to those in Western
Massachusetts, i.e., they are shallow fine sandy loams that are
sometimes underlain by shallow bedrock and sometimes underlain by
fragipans. Acidity and slopes are generally not as extreme in Western
Massachusetts,
Other soils in this area are sandier ("loamy sands" instead of "sandy
loams") and deeper (2-3 feet). These are well-drained soils (6 to 20
in/hr) , especially in lower strata (greater than 20 inches per hour).
Although slopes range from 0%-60%, runoff tends to be slow or moderate-
because of the permeability of the soil.
Also found in this area are deep muck soils that consist of decomposed
organic matter (up to 50%) found in depressions and flat areas that are
poorly drained (although the muck itself may be moderately permeable
(0,6 to 6.0 in/hr). Occasionally, the muck is overlain by a sand layer
(6,0 to 10 in/hr) which is deposited in these depressions from storm
drainage from the surrounding sandy soils.
The soils in the central and Middlesex area (the shallow, fine sandy
loams, the deeper sandier soils, and the muck) have pH values ranging
from 3,6 to 6.5, with the most common values ranging from 4.5 to 6.0.
Southeastern Massachusetts
Soil types in Bristol and Plymouth counties are highly variable, with
the most common being sandy loams. The range in common pH values is
similar to other parts of the state (pH 3.6 to 6.0). The potential for
water movement varies considerably;
- Rapid downward movement of water is likely in places where
sandy loams overlie layers of increasing particle size for (i.e.,
where there is water-sorted stratification of sands and gravels).
1-50
- A more complex situation is found in places where a sandy loam
with moderately rapid permeability (2.0 to 6.0 in/hr) overlies a
fragipan layer that slows water movement to 0.2 to 0.6 in/hr.
Just above the fragipan, there is a often layer of sand
(permeability of 6 to 60 in/hr) which provides a duct for lateral
movement of water which is blocked by the fragipan.
- In some places a fragipan can be found at a depth of 10 to 20
inches, and may be overlain for 7 to 9 months of the year by a
perched water table.
- As described above, deep, moderately permeable muck soils are
commonly overlain by a layer of sand that can encourage the
lateral movement of water.
Cape Cod
Most of the rights-of-way on the Cape are in the western section (the
"upper arm") of the Cape, where four soils are common:
- A loamy sand, overlying a gravelly coarse sand, which at a
depth of about 27 inches, changes into very deep layers of
gravel. The soil is rapidly permeable (6 to 20 in/hr) in the
upper layers and extremely permeable (>20 in/hr) in the gravel
substratum.
- A very deep coarse sand that is extremely permeable (>20 in/hr)
from its surface to its substratum.
- A fine sandy loam, similar to those found in most other parts of
the state, overlying a layer with more sand (a "loamy sand")
and then a gravel soil. Permeability ranges from moderate (2 to
6 in/hr) to rapid (6 to 20 in/hr) from the surface to the
substratum,
- A muck soil, similar to those discussed previously, found in
concave areas.
1-51
Lateral movement of water is less likely on the Cape than in other
places in Massachusetts, because of the propensity of water to move
downward. Runoff may also be less of a problem for the same reason.
The range of pH values is 3.6 to 6.0 on the Cape, as in many other
parts of the Commonwealth.
1-52
CHAPTER 7. RARE PLANTS ON RIGHTS-OF-WAY
Method for Inventorying
In order to avoid destroying rare plants on rights-of-way, applicators
must know the location of these plants. An inventory should be
conducted to identify and map the rare plants. To inventory the rare
plants found on existing rights-of-way, the following steps should be
taken: ..
1. A trained field botanist should identify categories of habitat along "*
the rights-of-way (i.e., wetlands, rocky slopes, calcareous areas) JS
through the use of geological, soil, vegetation, and topographical ^
maps, and field visits. J>
2. Plants should be collected in approximately 1/4 to 1/3 of each type
of habitat. The ability to recognize differences between similar
species (e.g., in the genus Cares) while collecting in the field is
essential for to an accurate inventory.
3. After proper identification, mounted vouchers should be kept in a
major herbarium (e.g., the New England Botanical Club, the
University of Massachusetts, etc.), so that a permanent record of
identities and localities is accessible to the interested public.
Also, a list of plants collected should be published by the botanist
in charge of the project.
4. Over the long term, an updated inventory can be maintained
though encouragement of scientific and educational activity on
rights-of-way. These activities, such as teaching several aspects
of plant ecology and collecting, could generate additional
information on new colonies of rare plants. Additionally, updated
lists of rare plants should be obtained on a regular basis from the
Massachusetts Natural Heritage Program (part of the Department of
Environmental Management) .
As shown in the following list, the endangered species are low-growing
species. Selective spraying or cutting should minimize the effect on
these species if care is taken to avoid contact with surrounding vege-
tation. To this effect, basal spraying may be less harmful than foliar
spraying, and herbicides with narrow spectrums (particularly those
1-53
effective only on woody plants) would be less harmful than those with
broad spectrums. The most important consideration may be the experi-
ence of the applicators in recognizing and avoiding known populations
of rare plants.
Inventory of Rare Plants
The attached list of rare vascular plant species in Massachusetts was
obtained from the Massachusetts Natural Heritage Program (Sorrie,
1983) and has been modified to include only those species likely to be
found on existing rights-of-way. Therefore, the attached list does not
include species exclusively found in habitats such as wooded areas,
shore areas (tidal, brackish, sandy, or muddy) or saltmarshes. The
decision to include or exclude species was based on published habitat
information by Fernald (1950) and Coddington and Field (1978). Ar-
rangement and nomenclature follow Kartesz and Kartesz (1980).
Information on the habitat and substrate pH is indicated by number or
letter codes as defined below:
1. Submerged in streams or ponds
2. Bogs, swamps, swales, or marshes
3. Peaty soil
4. River and stream banks
5. Lake or pond shores (sometimes in shallow water)
6. Meadows or grasslands
7. Shady rocks or ledges
8. Mountain slopes or summits
9. Sandy or gravelly soils
10. Dry exposed rocks or ledges
11. Roadsides, fields, or openings
12. Soils (not specified)
Substrate pH
a = acidic b = basic (i.e., calcareous)
Species for which habitat information was not available have been in-
cluded in this list, although the likelihood of their being found on
rights-of-ways is not known.
1-5^
TABLE 1-2
RARE PLANTS LIKELY TO BE FOUND ON
RIGHTS-OF-WAY IN MASSACHUSETTS*
Species Habitat**
EQUISETACEAE (Horsetails)
Equisetum palustre c 3
Marsh Horsetail
E. variegatum 3, 10
Variegated Horsetail
LYCOPODIACEAE (Clubmosses)
Lycopodium alopecuroides 2
Foxtail Clubmoss
L. carolinianum 3, 9
Carolina Clubmoss
L. selago 8
Fir Clubmoss
SELAGINELLACEAE (Spikemosses)
Selaginella rupestris 10
Rock Spikemoss
ISOETACEAE (Quillworts)
Isoetes acadiensis
Acadian Quillwort
I^, eatonii 5
Eaton's Quillwort
I^. macrospora 5
Lake Quillwort
OPHIOGLOSSACEAE ( Adder' s-tongue
Ferns)
Ophioglossum vulgatum
Adder' s-tongue Fern
*Adapted from Sorrie (1983).
**See text.
1-55
SCHIZAECEAE (Climbing and Curly Grass
Ferns)
Lygodiutn palmatum a 6
Climbing Fern
ADIANTACEAE (Cliff Ferns,
Maidenhair Ferns)
Cryptogramma stelleri b 7
Fragile Rock-brake
Pellaea atropurpurea b 10
Purple Cliff -brake
ASPLENIACEAE (True Ferns)
Asplenium montanum a 7, 12
Mountain Spleenwort
A. ruta-muraria b 10
Wall-rue Spleenwort
SPARGANIACEAE (Bur-reeds)
Sparganium minimum 4, 5
Small Bur-reed
POTAMOGETONACEAE (Pondweeds)
Potamogeton friesii b 4, 5
Fries' Pondweed
P. hillii 5
Hill's Pondweed
P. strictifolius b 5
Straight-leaved Pondweed
ALISMATACEAE (Arrowheads,
Water-plantains )
Echinodorus parvulus
Burhead
^. cuneata 4
Wapato
S. teres 4
Terete Arrowhead
X-$6
POACEAE (Grasses)
Aristida purpurascens
Purple Needlegrass
A. tuberculosa
Seabeach Needlegrass
Calamagrostis pickeringii
Reed-bentgrass
Dichanthelium acuminatum
var. wrightianum
Wright's Panic-grass
D. ovale var. addisonii
Commons's Panic-grass
D. scoparium
Broom Panic-grass
Eragrostis frankii
Frank's Love-grass
Muhlenbergia capillaris
Hair grass
Panicum gattingeri
Gattinger's Panic-grass
P. philadelphicum
Philadelphia Panic-grass
Paspalum laeve var. circulare
Paspalum Grass
Setaria geniculata
B ristly Foxtail
Sporobolis heterolepis
Northern Drop seed
9
9
a 3, 6
5
9
9
4
10
11
9, 11
6
9
10
CYPERACEAE (Sedges)
Carex alopecoidea
Foxtail Sedge
C. bailey i
Bailey's Sedge
C. bushii
Bush's Sedge
C, davisii
Davis's Sedge
D. formosa
Handsome Sedge
C. grayi
Gray's Sedge
C. lenticularis
Shore Sedge
C, livida var. gray an a
Glaucous Sedge
C, michauxiana
Michaux's Sedge
C. pauci flora
Few-flowered Sedge
C. polymorpha
2, 6
8
6
6
6
b 2
4, 5
2
2
2
9
1-57
Variable Sedge
C. schweinitzii
b
2
Schweinitz's Sedge
C. sterilis
b
2
Dioecious Sedge
C. tetanica
2,
6
Rigid Sedge
C. trichocarpa
b 2,
4
Hairy-fruited Sedge
C. typhina
b 2,
4
Cat-tail Sedge
C. walteriana var. brevis
2
Walter's Sedge
C. wiegandii
3
Wiegand's Sedge
Cyperus engelmannii
2.
5
Engelmann's Umbrella-sedge
Eleocharis equisetoides
5
Horsetail Spike-rush
E. erythropoda
2,
5
Redfoot Spike-rush
E. fallax
2,
5
Deceitful Spike-rush
E. intermedia
b
5
Intermediate Spike-rush
E. melanocarpa
5
Black-fruited Spike-rush
E. obtusa var. ovata
2
Ovate Spike-rush
E. quadrangulata
4,
5
Squarestem Spike-rush
E. tricostata
2, 4,
5
Three-angled Spike-rush
Psilocarya nitens
5
Short-beaked Bald-rush
P. scirpoides
2,
5
Long-beaked Bald-rush
Rhynchospora inundata
2,
5
Inundated Horned-rush
R. torreyana
4, 5,
9
Torrey's Beak-rush
Scirpus ancistrochaetus
2,
5
Barbed-bristle Bulrush
S. hallii
5
Hall's Bulrush
S. longii
2.
6
Long's Bulrush
S. pendulus
2
Pendulous Bulrush
Scleria pauciflora var. caroliniana
3, 9, :
10
Papillose Nut-rush
S, triglomerata
4, 5,
6
Tall Nut-rush
1-58
ARACEAE (Arums)
Arisaema dracontium 2, 6
Green Dragon
Qrontium aquaticum 2, 5
Golden Club
JUNCACEAE (Rushes)
Juncus biflorus 5
Two-flowered Rush
J. pervetus 2
Cape Cod Rush
Luzula parviflora ssp. melanocarpa 8
Black-fruited Woodrush
SMILACACEAE (Catbriers)
Smilax bona-nox 9, 11
BuUbrier
HAEMODORACEAE (Bloodworts, Redroots)
Lachnanthes Carolinian a 2, 3, 9
Redroot
IRIDACEAE (Irises)
Sisyrinchium arenicola 6, 9
Sandplain Blue-eyed Grass
ORCHIDACEAE (Orchids)
Aplectrum hyemale 8
Putty-root
Arethusa bulbosa 2
Arethusa
C, reginae 2
Showy Lady's Slipper
Listera cordata 2
Heartleaf Twayblade
Malaxis brachypoda 2
White Adder's Mouth
Platanthere ciliaris 2
Orange Fringed Orchis
P. cristata 2
Crested Fringed Orchis
P. dilatata 2
Leafy White Orchis
1-59
(m
p. flava var. herbiola 2, 6
Pale Green Orchis
P. obtusata 2
Bluntleaf Orchis
Spiranthes vernalis 6
Grass-leaved Ladies' Tresses
SALICACEAE (Willows)
Salix Candida 2
Hoary Willow
S. exigua 4, 5
Sandbar Willow
S. serissima b 2
Autumn Willow
BETULACEAE (Birches, Alders)
Alnus viridis ssp. crispa 4
Mountain Alder
Betula pumila 2
Dwarf Birch
FAGACEAE (Oaks, Beeches)
Quercus macrocarpa b 6
Mossy-cup Oak
Q. muhlenbergii b 12
Yellow Oak
POLYGONACEAE (Docks, Knotweeds)
Polygonum glaucum 9
Seabeach Knotweed
P. puritanorum 4, 5
Pondshore Knotweed
P. setaceum var. interjectum 4, 5,9
Strigose Knotweed
PORTULACACEAE (Purslanes,
Spring-beauties)
Claytonia virginica
Narrow -leaved Spring -beauty
1-60
CARYOPHYLLACEAE (Pinks, Sandworts)
Minuartia striata b 10
Rock Sandwort
CARYOPHYLLACEAE (Pinks, Sandworts)
Minuartia stricta b 10
Rock Sandwort
Moehringia macrophylla b 4, 5, 9
Large-leaved Sandwort
Paronychia argyrocoma var. 10
albimontana
Silverling
NYMPHAEACEAE (Water-lilies)
Nymphaea tuberosa 4, 5
Tuberous Water-lily
RANUNCULACEAE
(Buttercups, Crowfoots)
Clematis occidentalis b 10
Purple Clematis
Ranunculus circinatus 1
var. subrigidus
Stiff White Water-crowfoot
R. longirostris 4, 5
Beaked White Water-crowfoot
MAGNOLIACEAE (Magnolias)
Magnolia virginiana
Sweetbay Magnolia
PAPAVERACEAE (Poppies)
Adlumia fungosa 10
Climging Fumitory
BRASSICACEAE (Mustards)
Arabis lyrata 9, 10
Lyre-leaved Rock-cress
Cardamine douglassii 4, 5
Purple Cress
k;
1-61
PODOSTEMACEAE (Threadfoots)
Podostemum ceratophyllum
Threadfoot
CRASSULACEAE (Sedums)
Crassula aquatica
Pygmyweed
SAXIFRAGACEAE (Saxifrages, Currants)
Ribes americanum 2
Wild Black Currant
R. triste 2
Swamp Red Currant
ROSACEAE (Roses, Shadbushes)
Agrimonia pubescens b, 7
Hairy Agrimonia
Amelanchier bartramiana 8
Bartram's Shadbush
A. nantucketensis 5
Nantucket Shadbush
A. sanguinea b 12
Roundleaf Shadbush
Prunus pumila var. depressa 4, 9
Sandbar Cherry
Rosa acicularis 12
Prickly Rose
Sorb us decora 8, 11
Northern Mountain-ask
Waldsteinia fragarioides 4, 5, 11
Barren Strawberry
FABACEAE (Beans, Peas, Clovers)
Desmodium sessilifolium 9, 11
Sessile-leaved Tick-trefoil
Lespedeza violacea 11
Violet Bush-clover
OXALIDACEAE (Wood-sorrels)
Oxalis violacea 9, 10
Violet Wood-sorrel
LINACEAE (Flaxes)
1-62
Linum inter cur sum
3, 4, 5, 9
Sandplain Flax
L. sulcatum
11
Grooved Flax
POLYGALACEAE (Milkworts)
Poly gala senega
Seneca Snakeroot
b 2
CALLITRICHACEAE (Water-starworts)
Callitriche anceps 4, 5, 8
Northern Water-starwort
C. terrestrls 11
Terrestrial Starwort
EMPETRACEAE (Crowberries)
Corema conradii
Broom Crowberry
CLUSIACEAE (St. John's-worts)
Hypericum adpressum
Creeping St. John's-wort
H. stragulum
St. Andrew's Cross
3, 5, 9
9
CISTACEAE (Rockroses)
Helianthemum dumosum
Bushy Rockrose
VIOLACEAE (Violets)
Viola adunca
Sand Violet
V. brittoniana
Britton's Violet
9
3, 9
CACTACEAE (Cacti)
Opuntia humifusa
Prickly Pear
1-63
LYTHRACEAE (Loosestrifes)
Cuphea viscoslsslma 11
Blue Waxweek
Rotala ramosior 5
Tooth- cup
MELASTOMATACEAE (Meadow Beauties)
Rhexia mariana
Maryland Meadow Beauty
ONAGRACEAE (Evening -primroses)
Ludwigia polycarpa 5
Many-fruited False-loosestrife
L. sphaerocarpa 5, 9
Round-fruited False-loosestrife
HALORAGIDACEAE (Water-milfoils)
Myriophyllum alterniflorum 1
Alternate-flowered V^ater-milfoil
M. pinnatum 5
Pinnate Water-milfoil
APIACEAE (Parsleys, Angelicas)
Angelica villosa
Hairy Angelica
Conioselinum chinense
Hemlock Parsley
Hydrocotyle verticillata
Water Pennywort
11
2
4, 5
ERICACEAE (Laurels, Blueberries)
Pyrola asarifolia var. purpurea
Pink Pyrola
Rhododendron maximum
Great Laurel
b 2
2
GENTIANACEAE (Gentians)
Sabatia campunulata
Slender Marsh Pink
^. kennedyana
Plymouth Gentian
4, 5
4, 5
l-6k
ASCLEPIADACEAE (Milkweeds)
Asclepias vertlcillata 11
Linear-leaved Milkweed
HYDROPHYLLACEAE (Waterleafs)
Hy drop hy Hum canadense
Broad-leaved Waterleaf
BORAGINACEAE (Borages)
Onosmodium virginianum
False Gromwell
VERBENACEAE (Vervains)
Verbena simplex
Narrow-leaved Vervain
LAMIACEAE (Mints)
Agastache scrophularii folia 11
Purple Giant Hyssop
Blephilia ciliata 11
Downy Wood Mint
B. hirsuta 6, 11
Hairy Wood Mint
Scutellaria integrifolia 11
Hyssop Skullcap
Trichostema brachiatum b 12
False Pennyroyal
SCROPHULARIACEAE (Figworts)
Agalinis acuta 9
Sandplain Gerardia
Castilleja coccinea 3, 6, 9
Indian Paintbrush
Mimulus alatus 5
Winged Monkey-flower
M. moschatus 2, 4
Muskflower
Pedicularis lanceolata 2
Swamp Lousewort
Schwalbea americana 11
Chaffseed
1-65
Veronica catenata
Water Speedwell
Veronicastrum virginicum
Culver' s-root
b 12, 3
6
LENTIBULARIACEAE (Bladderworts)
Utricularla biflora 5
Two-flowered Bladderwort
U. fibrosa 5
Fibrous Bladderwort
U. subulata 3, 5, 9
Subulate Bladderwort
RUBIACEAE (Bedstraws, Bluets)
Galium labradoricum
Labrador Bedstraw
Hedyotis purpurea var. calycosa
Calycose Bluet
b 2
10
CAPRIFOLIACEAE (Honeysuckles)
Lonicera hirsuta
Hairy Honeysuckle
Symphoricarpos alb us var. alb us
Snowberry
Viburnum rafinesquianum
Downy Arrowwood
b 7
b 9
b 7
CAMPANULACEAE (Bluebells, Lobelias)
Lobelia siphilitica
Great Blue Lobelia
ASTERACEAE (Asters, Composites)
Aster con color 9
Eastern Silvery Aster
A. prenanthoides 11
Crooked-stem Aster
A. tradescantii 10
Tradescant's Aster
Eupatorium leucolepis 3, 4, 5
var. novae-angliae
New England Boneset
Gnaphalium purpureum 9, 5
Purple Cudweed
Petasites frigidus var. palmatus 2
1-66
Sweet Coltsfoot
Sclerolepis uni flora
Sclerolepis
Soli da go hispida
Hispid Goldenrod
S, macrophylla
Large-leaved Goldenrod
S. ptarmicoides (=Aster £.)
Upland White Aster
S. rigida
Stiff Goldenrod
5
4
8
b 9, 10
b 10
Im
73
1-67
i
(
(
APPENDIX II
INFORMATION ON INDIVIDUAL HERBICIDES
i;
II- 1
i
INTRODUCTION TO APPENDIX II
A number of people and organizations who commented on the report
requested more information on the EPA registration and reregistration
process, expressing concern that these chemicals are registered on the
basis of unreliable or nonexistant data. The following discussion pro-
vides general information on the EPA process and highlights some of the
issues which arise in evaluating the adequacy of that process. Addi-
tional information on the adequacy of the data base for each of the 14 K*
herbicides has been added at the end of each of the chapters which O
"n
follow . ,^
)>
The Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), as W
amended, provides authority for a number of Federal activities, includ- "j^
ing the issuance of experimental permits, the conduct of research on !!■»
biological controls, the certification of pesticide applicators, the j5
issuance of permits for special local needs, and the exemption of certain
pesticides from restriction in the case of an emergency. The most
important part of the Act, however, directs EPA to decide what pesti-
cides should be on the market, and what restrictions should be placed
S
on those that are allowed to be marketed. Encompassed by this broad J^
mandate are the specific sections in FIFRA devoted to registration, |h
reregistration, suspension, cancellation, and decisions about tolerances
(how much residue should be allowed on food), restricted vs. general
use (how much training the applicator should have) , toxicity category
(how strong the warning label should be) , reentry time (how much time
should pass before farmworkers are allowed back on the field where the
pesticide has been applied), and time-to-harvest (how soon after appli-
cation can the crop be harvested) .
Data which are considered in making these decisions include all of the
types of data included in this appendix, plus usage data (crops, pests,
application methods, seasonal timing, predicted geographic locations of
usage); applicator exposure estimates and safety recommendations;
recommended medical treatment in the case of emergencies; etc.
Although the registrant is responsible for generating these data, EPA
II-2
can also accept data generated by other sources. EPA has access to all
company data generated by the registrant in support of a registration.
Acceptable protocols for generating data have been outlined by EPA,
To over-simplify the process of hazard evaluation, the data submitted
by the registrant and other sources are compared to a set of criteria
which attempt to define 'unreasonable adverse effect' (the "RPAR trig-
gers"). Examples of these criteria include: a) a lack of an antidote,
b) evidence of carcinogenicity, teratogenicity, or mutagenciity , and c)
severe acute toxicity which protective measures cannot ameliorate. If
these threshold criteria are exceeded, the registrant is given a chance
to refute the conclusion that the pesticide causes an unreasonable
adverse effect. The registrant, at this point, submits additional data
which attempt to show that the adverse effect will not in fact occur, or
that the benefits of the pesticide outweigh the risk of the adverse
effect. If the registrant cannot show that either of these is true, the
EPA can begin the process of cancelling the registration of the pesticide
(or deciding not to register it in the first place) . EPA then acts as an
advocate in a judicial process, attempting to prove that the pesticide
will have an unreasonable adverse effect, while the registrant attempts
to prove the opposite, and the public is provided a chance to contrib-
ute data and opinions.
At the present time, the required data and the protocols outlined for
generating these data are fairly extensive and thorough. However, this
was not always the case. Most of the pesticides currently on the
market were registered before the current registration requirements
were in effect (the largest increase in data requirements took place in
1972) . Many pesticides were in fact registered before EPA came into
being in 1970; i.e., they were registered by USDA and 'grandfathered'
into the set of products currently registered by EPA. In general,
pesticides which were registered before 1972 do not have adequate data
(many have no data) on a number of important topics, including carcin-
ogenicity, teratogenicity, and mutagenicity. Even some registered after
1972 have inadequate data bases because acceptable protocols were not
defined by EPA for several years. Thus, it is not possible to
II-2.1
state that a pesticide is "safe" because it is registered by EPA, since
many of the pesticides currently on the market have not been reviewed
by EPA, nor have they been tested to determine their potential hazard.
The obvious response to this situation is the suggestion that pesticides
which have an inadequate information base should be removed from the
market until data can be generated which show the pesticide to be safe;
i.e., the general population should not be exposed as "guinea pigs" to
chemicals of unknown safety. However, when Congress extensively "•*
amended FIFRA in 1972 and in subsequent years, no mechanism was j3
given to EPA to remove a pesticide from the market because of inade- ,j^
quate data. To suspend or cancel a pesticide, EPA must show that the )>
pesticide causes an unreasonable adverse effect. The burden of proof, lU
in other words, is on the Agency to prove harm, rather than on the *^
registrant to prove safety. (The only exception to this is that, once iS
EPA officially requests information, the company has 90 days to relay jTI
c
its intention to provide those data . If the company does not respond in
90 days, EPA can move to suspend the pesticide. On the other hand,
if the company responds within 90 days, there is no legal deadline for
the subsequent submission of those data, and there is no way that EPA iP
can remove the product from the market while the data are being gener- IJU
ated.) Aside from the burden-of-proof problem, suspension of products
with an inadequate data base poses another difficulty. Congress built
in a strong disincentive for suspension decisions by stating that EPA
must find the funds from within its own budget to remove the sus-
pended product from the marketplace and dispose of it safely. Sus- 1
pending the 35,000 pesticide products registered by USD A (prior to
1970) would therefore be financially impossible, even if EPA had statu-
tory authority.
Recognizing the need to reexamine the products registered by USD A, Ij
Congress included in its 1972 amendments of FIFRA a requirement that j
EPA reregister these products by October 21, 1976. A number of
activities, including a need to organize the old USDA files, prevented
the reregistration effort from getting underway until 1975, when a few
EPA people started going through the data on the 35,000 products.
II-2.2
At the same time, EPA was coming under pressure from Congress about
the length of time necessary to conduct registration reviews. Single
registrations on new products were taking years and many hundreds of
man-hours to accomplish. Trying to meet the 1976 deadline, and know-
ing the resources required for a thorough review of data, a decision
was made to concentrate on identifying and filling data gaps. As part
of a Senate hearing on the matter in 1976, however, an independent
toxicologist questioned the validity of the existing data in the old USDA
files. In a report issued by the Senate Subcommittee on Administrative
Practice and Procedure in December 1976, EPA was accused of negli-
gence in its review of data for reregistration. EPA officials, mean-
while, were attempting to educate Congress, GAO, and its other accus-
ers about the time and money necessary to review the 35,000 products
with attention equally as thorough as that given new registrations. (At
that time, EPA was registering less than 50 new pesticides a year,
although the numbers varied considerably upon inclusion of different
types of reviews, such as label changes, additional tolerances, etc.)
In 1976 and 1977, EPA made requests for significant increases in staff
and budget to handle reregistration. Finally, a small budgetary
increase was provided for that purpose in 1978.
By this time, EPA had begun defining what is now known as the Regis-
tration Standards program. To make its task more manageable, EPA
decided to concentrate not on the 35,000 separate products but on the
514 active ingredients in those products, with decisions on products
grouped according to common active ingredients. According to the
current approach, each standard attempts to:
1) Review the validity of the existing data and identify data gaps,
which must be filled before the products can be reregistered.
2) Decide what products will be reregistered, and what restrictions
will be imposed.
3) Decide whether the existing food tolerances of the product
should be changed.
4) Decide what the label for each product should say.
II-2.3
This re registration effort is now well underway, and is expected to be
completed in 10 to 15 years at a cost of several hundred million dollars.
Meanwhile, questions about the validity of registration data were being
raised by inspections of the laboratories generating those data. FDA
discovered "serious deficiencies" (including fraudulent data) in a rou-
tine inspection of one of the laboratories of Industrial Bio-Test Labo-
ratories, Inc. (IBT). In EPA, this discovery led to a moratorium ^
placed on any registration applications which included data developed D
by IBT. In 1977, registrants were notified that they had to determine ,j^
the validity of IBT tests according to EPA validation guidelines. The ^^
results of the registrant's evaluation (but not the raw data) would be
trant so that EPA could conduct spot-checks of the registrants' audits.
These spot-checks uncovered a number of problems in the audits of the
registrants, and EPA and FDA (in conjunction with the Canadian gov-
The review of IBT studies was conducted between 1978 and 1983. It
consisted primarily of 1) a validation review; i.e., do the raw data
support the information in the fined report, 2) an evaluation review;
i.e., do valid studies conform to agency guidelines, and 3) a data gap
review; i.e., is there another existing study in the chemical's data base
to substitute for an invalid study. To save time, EPA eventually
dropped the data gap review, assuming instead that an invalid IBT
study had to be redone unless the registrant could come up with a
substitute.
Midway through this review process, a number of decisions were made.
The moratorium on registrations containing IBT data was lifted except
for those registrations which depended on validation of an IBT study
considered essential or critical to the evaluation. Thus, the normal
review process could begin again on registrations which contained.
1^
reviewed by EPA, which would make the final determination of validity. 'h
After more problems were uncovered in an EPA /FDA inspection of two iS
other IBT labs, EPA decided to request the raw data from the regis- hi
5
c
IDS
ernment) decided to review each audit with the accompanying raw data. [P5
'?3
II-2.4
for example, an IBT-generated acute toxicity study, during the time
that that IBT study was being validated or replaced. It was also
decided that, if invalid IBT data comprised an entire data base, EPA
could consider the product for cancellation. Finally, if it was dis-
covered, in the replacement of an IBT test or by other input, that the
pesticide had an adverse effect that had not been mentioned in the
original application, EPA could expedite the regulatory process and
initiate an intensive risk /benefit review or formal hearings on the status
of the registration.
At the present time, the review of the IBT studies is nearly complete,
and the remaining effort will be devoted to replacing the IBT studies
(i.e., tracking the registrants' commitments to replace the studies). Of
the 801 IBT test reviews, 74% were found to be invalid. A report
written by EPA at the end of the review process concluded with the
following comment:
The IBT case caused serious concern and uncertainty
about the potential hazards of the hundreds of pesticides
involved, both for EPA and the public. Although it was
advocated by some that all 212 pesticides tested in whole or
in part by IBT be removed from the market pending retesting,
that option is not available under current law. The regula-
tory response authorized by FIFRA requires valid evidence of
risk, as opposed to a lack of information, before removing a
product from the market, and allows for replacement of inade-
quate data. As we reach the final resolution of the IBT
problem, it appears that this response was appropriate and
adequate to deal with this event.
(By this, we can presume that EPA did not uncover a significant num-
ber of previously unknown adverse effects that would have warranted
suspension of the products while the review was being conducted.)
Seven of the herbicides discussed in this report had registrations
supported by some IBT data: atrazine, dicamba, diquat, glyphosate,
metolachlor, picloram, and triclopyr. For each of these chemicals.
Appendix II contains a brief discussion of the tests done by EPA and
their status in regard to replacement. In general, most of the IBT
studies have already been replaced. Dicamba remains as the one herbi-
cide with a large number of data gaps still imposed by the IBT scandal.
II-2.5
In 1977, EPA and FDA established a joint audit program to make sure
that another IBT situation has not already happened, and to make sure
another does not happen in the future. Inspections are now made of
the facilities, procedures, and staff qualifications of laboratories
generating health effects data. Additionally, about 60 audits a year are
conducted to see if the raw data concur with the reported results.
According to EPA, "the large majority of laboratories" have been found
to be acceptable, conducting scientific eilly valid tests in accordance with
current standards. However, among the audits conducted between 1977
and 1980, 25 of the 82 laboratories audited were found to have serious
deficiencies, including falsified research reports, contamination of feed
with chemicals being investigated in other tests, and most frequently,
improper record keeping.
The problem of public confidence in registration data has been further
compounded over the last decade by an attempt by Monsanto and other
large pesticide companies to hmit public access to those data. These
companies state that the public availability of registration data allows
so-called "me-too" companies to register products after the patent runs
out, or in foreign countries where U.S. patents do not apply. By
making the data available to the public, Monsanto and others argue that
the original registrant essentially subsidizes the other companies which
want to make the same product. In response to these concerns, Con-
gress has tightened the requirements for compensation by "me-too"
companies for use of data submitted by the original registrant. How-
ever, Monsanto and others maintain that the problem still exists in
regard to 'subsidizing' competitive registrations in foreign countries.
There are some who believe that an additional reason for withholding
data from the public is the fear that some environmentalists will search
through the data looking for problems with which to challenge EPA's
decisions .
The conflict over the availability of data also affects the review of data
by the Commonwealth of Massachusetts. Companies want assurance that
data submitted would remain confidential and only be examined by
II-2.6
qualified individuals. During extensive deliberations on this subject in
the late 1970s, the Massachusetts Pest Control Board objected to these
conditions, stating that the Commonwealth needed to provide information
to a number of queilified people in the public, academic, and govern-
mental sectors. Since the resolution of this question was pending in
court, the Commonwealth decided not to set up procedures for protect-
ing the proprietary nature of data submitted by companies. As
described in the previous discussion of laws and regulation, the
Supreme Court decided in June of 1984 to allow public disclosure of
data provided in support of all FIFRA registrations, with certain limited
exceptions (e.g., data on inert ingredients) similar to those exceptions
originally included in the 1972 revisions of FIFRA,
,j * ♦ *
'«
<
I The following discussion of herbicide data does not attempt to be a
^ complete review of all available information. Because of time and bud-
get constraints, only immediately available information was used. The
contract for this work stated that secondary-source material (reviews of
original studies) would provide the base of information for this report.
Accordingly, a computer search of secondary-source material was under-
taken and reports which were in the Boston area were identified and
obtained. Reports which were considered to be particularly important
were obtained by mail. The files of individual task force members were
searched. Finally, requests for information were made of the companies
which manufactured the 14 herbicides. The response of the manufac-
turers was uneven; however, the manufacturers which did respond sent
both positive (i.e., showing no adverse effect) and negative data,
although the former predominated.
Upon assembling the secondary-source material, each topic was reviewed
to determine whether primary-source information (the original studies
written by the investigator who conducted the work) was needed to
supplement the information gathered so far. The following data bases
were searched: BIOSIS, CHEM ABSTRACTS, AGRICOLA, MESH (Index
Medicus, Medlars), and TOXLINE. Key studies were identified by: 1)
II-2.7
the attention given to them in the related secondary-source material, 2)
their availability in the Boston area, and 3) the date of publication.
As can be seen in Appendix II, the adequacy of the data base varied
considerably among the herbicides. Because many of the herbicides
have such a poor data base, data generated by the manufacturer was
included. This decision was criticized by several people who reviewed
the draft GEIR, who felt that the incorporation of manufacturer's data
jeopardizes the reliability of the conclusions drawn. Some felt that the
manufacturer would be likely to falsify information in order to obtain a
registration from EPA, The IBT scandal contributes to this fear. It is
the authors' experience, however, that such falsification is the excep-
tion rather than the rule, and that most laboratories, whether company-
owned or under contract, do not falsify data. Faced with evidence of
adverse effect, most companies will not try to trick EPA into registering
a product, if only because the fincincial risks are too high. The large
initial costs of meinufacturing and marketing the herbicide, plus the
registration costs, would all be lost as soon as an independent
researcher discovered the adverse effect and the RPAR mechanism was
triggered.
Some reviewers also criticized the incorporation of compciny data because
the information had not been peer-reviewed. However, the EPA regis-
tration process is as thorough as normeil peer reviews. An IBT scandal
does not disprove this since complete falsification of data is difficult to
detect by any kind of peer review, as evidenced by the number of
recent examples of complete data-falsification in the open literature.
A number of people who reviewed the draft EIR criticized the way that
conclusions were drawn about the herbicides. Most of the criticism
focused on the summary statements, contained in the main body of the
report, regarding the toxicity of the herbicides. The concern was over
statements regarding the lack of data which showed adverse effect.
These reviewers felt that statements such as "available data showed no
evidence of carcinogenicity" were misleading in light of the paucity of
data available. These criticisms are valid, and a number of statements
II-2.8
have been revised to provide more emphasis on the lack of data and the
uncertainty regarding potential adverse effects.
The suggestion was made by some reviewers to only consider studies
which give positive results; i.e., which show adverse effect. The
reasoning behind this suggestion is usually that:
1) The small statistical sample involved in any toxicity test makes
a negative result less meaningful than a positive one.
2) The lack of effect means only that the investigator did not see
what he or she was looking for. Some effects, such as subtle or latent
signs of biochemical or histological changes, need specially designed
studies, and no tests are yet available for some effects, such as nau-
sea, fatigue, headache, and minor central nervous system abnormalities.
Many chemicals, of course, do not cause adverse effects; negative data
are the only way to show that this is true. The increased reliability of
positive results, however, should cause the reader to question instances
when there are only a few studies and these are negative. This is
particularly true when the type of test is likely to produce false neg-
ative or false positive results.
II-2.9
A. AMINOTRIAZOLE
1. INTRODUCTION
Aminotriazole is the common name for the herbicide 3-amino-
1,2,4-triazole from American Cyanamid Company (Thomson, 1975). It is
also called Amitrole , Amitrol , ATA, Azolan , Weed-Ar , Weedazol ,
® ® ® ®
Cytrole , CytroAmitroleT , Herbizole , and Azole (Thomson, 1975;
TRW, 1981). Its chemical structure is
C-NK
Aminotriazole is a stable, white crystalline solid (Carter, 1969). Other
relevant physical and chemical characteristics are described below in the
discussion of the fate of aminotriazole in soil and water.
2. TOXICITY
Acute Toxicity
Low acute toxicity values have been reported in a number of studies.
Weir et al. (1958) reported an oral LD_-^ value of 14,700 mg/kg for mice
and 25,000 mg/kg for rats. Washington State University and the U.S.
Department of Agriculture (1971) assessed the toxicity of Amitrole-T, a
formulation of amitrole that contains ammonium thiocyanate as an
activator, and reported an LD value of 5000 mg/kg to rats. The
same study reported a dermal LDrr, value of greater than 10,000 mg/kg
for rabbits. Norris (1976) stated that LD-^ values ranged from 5000 to
25,000 mg/kg. Intravenous administration was studied by Weir et al.
(1958), who reported that concentrations of 1600, 1750, and 1200 mg/kg
had no effect on mice, cats, and dogs, respectively.
II-3
Intraperitoneal administration results in moderate toxicity of
aminotriazole. The National Institute of Occupational Safety and Health,
as cited in Lewis and Tatken (1982), reports that the intraperitoneal
LD^Q is 200 mg/kg.
Subacute /Subchronic Toxicity
Adverse effects have been reported in subchronic toxicity tests. In a
study reported by Weir et al. (1958), rats were fed 1000 and 10,000
ppm for 63 days. Altered weight gain and fatty metamorphosis of the
liver were observed. Jukes and Shaffer (1960) reported enlarged
thyroid glands in rats fed 60 or 200 ppm aminotriazole for two weeks.
The study associated this effect with a decrease in the uptake of
radioactive iodine. Englehorn (1954) did not observe these changes at
15 or 30 ppm (no duration of exposure is given in a review by Durham
and Williams, 1972).
Special Studies
Carcinogenicity Available data suggests that aminotriazole can be
considered a carcinogen. Aminotriazole was used as a positive control
in a carcinogenicity test by Innes et al. (1969). In that study, male
and female mice (C57BL/6 x C3H/Anf and C57BL/6 x AKR) were fed
1000 mg/kg aminotriazole by gavage on days 7-28 of age. Thereafter,
the mice were fed a dietary dose of 2192 ppm for 18 months.
Carcinomas of the thyroid were found in 64/72 (89%) of the mice. In
the C57BL/6 x C3H/Anf cross, hepatomas were found in 16/18 ((89%) of
the males and 18/18 (100%) of the females, compared to 8/63 (13%) and
0/71 (0%), respectively, in untreated controls. In the C57BL/6 x AKR
cross, 16/18 (89%) of the males and 17/18 (94%) of the females had
hepatomas, compared to 4/72 (6%) and 1/65 (2%), respectively, in
untreated controls.
Aminotriazole was used to confirm the ability of a new test system to
detect carcinogens (Inoue et al. , 1981). In this test, hamster embryo
cell colonies were exposed in culture to aminotriazole for 8 days.
Aminotriazole induced the expected morphological transformations at all
II-4
concentrations — 10, 50, and 100 yg/ml. No such transformations were
seen after exposure to phenyl salicate as the negative control.
Tsuda et al. (1976) found a statistically significant increase in invasive
lesions and papillary adenoma nodules after administration of 2500 ppm
aminotriazole in drinking water to Wistar rats. Invasion of follicular
tissue through capsules into adjacent stromal tissue (considered to be
evidence of malignancy) was observed in 19% of the treated rats,
compared to 0% in the control group. Papillary adenoma nodules were
found in 3% of treated rats, as contrasted with 0% in control groups.
As reported by an lARC Working Group (1974) that evaluated the
carcinogenic risk of a number of industrial chemicals, several studies
have indicated tumor induction by aminotriazole. In addition to the
studies mentioned above, this report cites a study by Jukes and
Shaffer (1960), who found dose-related induction of thyroid adenomas
after administration of aminotriazole for 104 weeks at the relatively low
levels of 10, 50, and 100 ppm. Thyroid adenomas developed in 1/10,
2/15, and 17/26 rats treated at the three dose levels. No tumors,
except for a cystic follical, were found in control rats. Similar results
were found by the Food Protection Committee (1959) as cited by Hodge
et al. (1966). In that study, the same doses were administered (10,
50, and 100 ppm), and thyroid adenomas were observed in 1/27, 3/27,
and 15/27 rats, respectively. In a third study (reported by the lARC
Working Group), Napalkov (1969) found thyroid tumors in 7/22 male
rats and liver tumors in 12/23 male rats (data on female rats were not
provided) after administration of aminotriazole in drinking water at a
rate of 20-25 mg/ day /rat or in the food at 250 or 500 mg/ day /rat.
A secondary source, Norris (1976), states that when rats were fed
dietary concentrations of 50, 100, and 500 ppm aminotriazole for 476,
730, and 119 days, respectively, no adverse effects were seen at the
lowest and highest doses, but that thyroid adenomas and
adenocarcinomas were produced at 100 ppm. No primary source was
provided. Another secondary source (USDOE, 1980) states that
II-5
"thyroid tumors began appearing in rats fed at 100 ppm for 68 weeks."
No primary source was provided. The limited number of studies
available on aminotriazole show no teratogenic effect, although more
study is clearly needed.
Teratogenicity /Reproduction Aminotriazole does not appear to be a
teratogen in mice. When aminotriazole was administered subcutaneously
to mice at a level of 464 mg/kg (in 0.1 dimethyl sulfoxide) from day 6
to day 14 of gestation, no significant increase in malformations was seen
among the offspring of treated mothers (USDHEW, 1969).
Aminotriazole has caused adverse effects in egg injection studies.
Dunachie and Fletcher (1970) noted a 25% decrease in hatching at 100
ppm aminotriazole. Using high concentrations (20-40 mg/egg),
Landauer and associates (1971) found up to 50% embryotoxicity after 96
hours of incubation. Increases in abnormalities, principally in formation
of the beak, were noted at doses of 10 to 40 mg/egg. Treatment with
doses of up to 2 mg/egg were without effect. A subsequent study
(Leindauer and Salam, 1972) found a slightly reduced incidence of terata
when the aminotriazole was dissolved in dimethyl sulfoxide instead of
water. The nature of the solvent, however, did not affect
embryomortality, which was 60% with both solvents. The differing
responses due to solvent are most likely attributable to solvent effects
on cellular penetration and on distribution to sensitive sites.
It should be noted that chick egg studies are not considered meaningful
in assessing risk to humans because of the absence of anatomical and
physiologic maternal-fetal relationships during incubation.
Mutagenicity Although most of the studies shown in Table II- 1 show no
mutagenic activity of aminotriazole, the need for more study is indicated
by the results of Kubinski et al. (1981) , who found mutagenic activity
when liver enzymes were added to a DNA cell-binding assay using E.
coli.
Summary
An evaluation of important toxicity data is provided at the end of
this chapter.
II-6
sO
Cu
<u
^1
o
2 rt
;h
S m
3
CTJ ^
0
cd 0
in
J w
^s DO
•vO 5-1
C^ (U
<u
• — • 9 #■•*
a
■♦->
•I— > (u
o
2 C/3
oo
(U
nJ
0)
C
c^
/— V
nO
,-^
- — ^
vO
c^
00
r-
1— (
fO
00
r^
o^
r^
o^
00
c^
o^
rH
o^
1— 1
o^
o^
1— (
n>
0}
s
c
•f-i
pa
'— : rt -(->
rt
rt
(U
^ '-I rt
^ cO rt
0)
u
U
en
rt
c
o
en
u
a
.1-1
V4
en
rt
• «-<
n
^
^
0
rt
A
U
en
<
CQ
s
U
cn
CQ
<
o
<
on
o
I— I
H
en
w
H
H
u
I— I
z
o
<
H
P
IS
o
U
3
en
a;
Pi
S S
o o
I I
0\«>
I— I o\o
I CM
(N] .
• O
O V
I I
u
«J -,
^ <u
en
O -M
Rl
s-c
iU
&0
^
"U ,A ^
en
(U
i-H en 3
O 3 .5
r— 1
o
£ 't; '^
e
0- o
bO 00
GO
GO
^^"^
3.
0)
3. 3.
3.
3.
«= ^ ^
tn
>
o o
o
O
,_
o\o
LTi rt en
r-
0
o o
o
o
3.
-^
^ ^ ^
r— 1
^
o o
o
o
•
r-l 0 T3
esi
rt
(Nl (M
04
r— I
LD
O
I
^3
a
en
0)
rt
r— 1
en
• il
>^
^
cn
a
o
.)->
en
en
O
<u
u
H
Q
(0
(U
>^
o
o
a
1— t
c
a
rt
52 <^
en ^
73 §
i^ a
no en
<u —
en O
en
C
rt
1—1
3
en
I— t
•1-1
DOl
a;
en
<
C
O
.1-1
H->
rt
+j
3
a
>
o
DO
c
O J"
CO
<
'o
o
•1-1
o
C
3
3 en
T3
C
O
2
rt
en
en
rt
en
en
■M
D
•o
O
3
>>
en
a
o
en
3
a
^
0)
• rH
u
u
■(->
rt
en
CQ
rt
13
c
o
a
I— I
en
m
tn
(U
u
u
o
in
vO
sO
c^
p»
CT^
0^
i-H
l-l
•-^
Sa^
&fi
^ Qfl
Vi
'"^
0 V^
H)
^■^ vO
r- <u
CO r-
(U
1— 1 •^-'
u
a
>_'
. a
•
-^■^
a
^ rt
0
«j
-«->
73
<U TJ
ford
;a an
•c.^
1 ^
0
0 4:
rt 0
w
2 w
fQ in
00
•IH
CO
•l-l
c^
a^
1— 1
■^^
CJ
u
c^
di
a*
^
i-i
•»-»
v-'
c
3
•
l-H
a
(d
^
-0
c
rt
g
E
CO
u
73
2
C
0
<
cu
f
o
<
l-H
0
D
Z
Z
2
1— 1
<
Z
0
• •
0
W
H
en
r-t
w
1
1— 1
H
l-H
CQ
0
<
HH
H
z
w
0
<
H
0
IS
en
C
e
6
o
O
3
CO
S
cn
CO
<u
•l-l
O
u
I I
(4
•IH
1— 1
l-H
l-H
0
0)
u
fl
0
«J
E
r— 1
•l-l
•C
rt
u
W
•1^
$H
»
0)
cn
E
cn
<
W
CO
LD
I I
o
o
o
.1-1
u
.1-1
u
cn
CO
a
>
CO
O
O
1—1
I
o
no
p.
in
>^
ni
CO
CO
a
S
^
•<a*
n
H
§
CJ
•S
0 GO
E
CCS
J2
t
cn ^
3
•f-l
1
1— 1
1—1
c 0
0
(U
ni .ri
0
•l-l
0
H-> Sh
&c
U
d (U
$H
CJ
<
z
II m
bact
cd
I— 1
cn
Q
d^
W
u
■4->
(U
u
0)
H->
CTJ
u
• rH
T3
• iH
CO
(U
(0
,£!
H->
c
<u
$H
CCJ
Oh
■I
3. MOBILITY AND PERSISTENCE
Fate in Soil
It is difficult to summarize the fate of aminotriazole, because its
behavior appears to depend greatly on the nature of the soil. Although
most chemicals show this variation with soil type, aminotriazole seems
particularly variable in regard to both mobility and persistence. In
general, aminotriazole can be expected to be mobile in sandy soils but
immobile in organic ones or in soils with high clay content.
Kaufman et al. (1968) found that 40% of applied aminotriazole was
adsorbed onto inorganic soils, while only 3% was adsorbed onto an
inorganic soil. Leaching was found to occur readily in sand or sandy
loam, but much less readily in clay, clay loam, or soil with a high
organic content (Sheets, 1961). Marston et al. (1968) found that
aminotriazole adsorbs readily and tightly to soils having a high base
exchange capacity and a high percentage of organic matter. Sund
(1956) also found adsorption to be dependent on the soil's base
exchange capacity, and that aminotriazole may adsorb to soil colloids or
complex with metallic ions (such as nickel, copper,, iron, and
magnesium) .
Day et al. (1961), on the other hand, stated that adsorption was not a
function of the base exchange capacity or the soil classification of 55
California soils. These authors conclude that aminotriazole would
readily migrate since it is highly soluble in water, and the adsorbed
aminotriazole can be released with sufficient infiltration of water.
Specifically, Day and his colleagues found that although 20%-50% of the
aminotriazole was adsorbed to a variety of soils, the bound aminotriazole
could be released by repeated percolation of water through the soils.
Both volatilization and photodegradation are believed to be insignificant.
The volatility of aminotriazole is stated as being low (no data
provided) , and the herbicide is considered to be stable under
ultraviolet radiation. (Norris, 1971; Day et al. , 1961; Ercegovich and
Frear, 1965; Plimmer et al. , 1967).
II-9
It is generadly accepted that aminotriazole has a low to moderate per-
sistence in soil, depending on soil type and conditions such as soil
temperature and pH (TRW, 1981). Persistence increases with colder
temperatures and decreases if the pH deviates above or below neutral
(Ercegovich and Frear, 1965). The half-life of aminotriazole in a forest
litter was found to be 5 days (Norris, 1970a). Burschel and Freed (no
date provided) found a half-life of 6 weeks in a Chehalis loam soil and
a breakdown rate of 1.31 yg/g soil/day. Freed and Fxirtick (1961)
found that aminotriazole which had been applied at rates of 1-2 lb /acre
on three Oregon soils could not be detected 2 months after application.
After 6 days, recovery of aminotriazole from Hagerstown silt loam soil
was 58%, 8%, and 0% from air-dried soil, soil with 15% moisture, and soil
with 30% water, respectively (Gangstad, 1982; no primary source given).
It is uncertain whether the primary route of degradation is microbial or
chemical. Limited success has been obtained in isolating soil microor-
ganisms that degrade aminotriazole (TRW, 1981). The exhibition of a
lag phase, typical of microbial degradation, indicates the possible
importance of microorganisms. Additionally, it has been found that the
degradation of aminotriazole almost stops if the soil is autoclaved (Day
et al., 1961; Ercegovich and Fresur, 1965; and Kaufman et al., 1968).
Microbial breakdown may not be directly responsible for degradation,
but may enhance or provide the conditions necessary for chemical
degradation. Chemical degradation is suggested by the evolution of
CO- from aminotriazole in the presence of free radicals (Plimmer et al.,
1967; Kaufman et al. , 1968). Whether the mechanism that opens the
triazole ring is chemical or microbial, the resulting products (urea,
cyanamide, and nitrogen) will be readily metabolized by microorganisms
(Carter, 1975).
Persistence in Water
Available information suggests that aminotriazole does not persist in
streams for more than a week (Norris et al. , 1967; Marston et al.,
1968). Norris (1967) showed that when aminotriazole was applied to 260
acres of a forested land at rates of 2 lb /acre, residual levels peaked
within 2 hours and were undetectable by the third day. Residues of
422 ppb and 6 ppb were found after 0.17 hours smd 8 hours.
11-10
respectively. In the study by Marston et al. (1968), 100 acres were
treated with aminotriazole at a rate of 2 lb/acre. A maximum concen-
tration (155 ppb) was attained 30 minutes after beginning application.
After 2 hours, the aminotriazole concentration was 26 ppb; within 6
days the herbicide was no longer detectable.
It should be noted that these studies are difficiilt to interpret without
information on dilution rates or herbicide sinks (degradation, accumu-
lation in sediment, upteike by plcints, etc.).
Indicators of Potential Ground Water Contamination
Table II-2 provides information on parameters associated with the mobil-
ity of aminotriazole. These parameters, and their associated thresh-
olds, have been suggested by EPA for use in assessing the potential
for pesticide contamination of ground water. A discussion of these
parameters and thresholds, and the methods for arriving at designated
values for individual herbicides, is presented in the main body of the
report as part of the discussion of the fate of herbicides in the envi-
ronment .
Toxicity Data Evaluation
Sufficient data exist to consider aminotrizole a carcinogen. However,
available studies cire insufficient to draw a conclusion about teratogenic
effects. Additional studies regarding mutagenicity are needed because
of the potential for activation by liver enzymes. At the time the draft
GEIR was issued, a registration standard was being prepared by EPA to
identify data gaps. However, that effort was terminated and a "special
review" of aminotriazole was initiated in 1984, indicating a cause for
concern had been found. The Scientific Advisory Panel, which guides
EPA, was provided information on the chemical in June 1984. No fur-
ther action has been taken by EPA at this date. The Commonwealth of
Massachusetts is currently considering regulatory action regarding
aminotriazole; a decision is forthcoming soon.
No data in support of the registration of aminotriazole were generated
by IBT.
11-11
TABLE II-2
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
AMINOTRIAZOLE
i
Indicator
Solubility
K
oc
Speciation at pH 5
Hydrolysis half-life
Photolysis half-life
Vapor pressure
Value for Aminotriazole Threshold
280,000 ppm at 23°C
0.059
Neutral or cationic
ND*
ND*
Non-volatile
>30 ppm
<300-500
Anionic
(negatively charged)
>6 months
>3 days
-2
<10 mm Hg
* ND = no data
(
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Aminotriazole appears to be non-toxic to test birds. Various studies by
Heath et al. (1972), Hill et al. (1975), Maier-Bode (1973) and Pimental
(1971) show LDj.. values for mallard ducks to be greater than 2000
mg/kg, and LCj... values for mallard ducks, pheasants, Japanese quail,
and ring-necked pheasants to be greater than 5,000 ppm in feed for 5
days. These data are summarized in Table II-3.
t
11-12
0)
u
o
o
c^
o^
I— 1
^^
(U
<u
^
y^^
^^^
^^
y^
•♦-»
rv]
(SJ
(Na
CO
J3
t^
„,-»
c^
^^
r^
,^~^
f-
nJ
a^
(NJ
o^
LO
c^
tn
o
/-"^
;^
t— t
r-
1— (
r~
t— 1
r^
e— I
c— (
o
^— '
o^
^-^
cr^
>— '
o^
^-^
C^
r— t
rH
1—1
O^
TS
•
«- _ -*
•
*- -*
•
■^^
•TO
p^
1— 1
1 )
r— 1
>— '
c
rt
•
nJ
•
rt
•
0
,
rt
-M
1— 1
■M
rt
■M
rt
CQ
03
^
(U
a;
(U
1
■<-»
•«->
-M
4^
!h
C
J3
<u
^
(U
^
(U
•t-i
OS
0)
•M
+->
■M
S
u
3
l-H
1— H
0)
1— 1
• r-l
2
O.
H
OS
X
E
K
3:
X
CO
I
CQ
Q
t-H
CQ
O
E-t
O
<
I— I
H
O
2
<
O
H
H-l
o
I— I
X
o
3
en
05
00
a
o
o
o
(VJ
A
e
a
o
o
o
in
A
en
H
S
a
a
o
o
o
A
E
a
a
o
o
o
LD
A
E
a
p-
o
o
o
tn
A
o
o
o
o
«r>
LD
in
un
O
U
U
U
o
tn
J
J
J
J
Q
>>
>^
>^
>^
1-^
OJ
OJ
rt
fd
1
•T3
1
1
1
1
Lf)
1
in
1
in
1
in
CO
r-l
I
cn
^
u
3
-a
en
^3
0)
u
u
(U
I-H
a
nJ
w
2
fl
(Tl
en
(«
0)
^
1— 1
Cu
(ti
3
'^
cr
0)
en
^
0)
-*j
u
01
C
(U
(U
rt
i::
c
en
1
aJ
rt
bO
a
(U
c
ns
js
•l-t
•r>
CU
^
Fish
Aminotriazole appears to be non-toxic to a variety of fish. A study by
Bond et al. , (1959) gave a 48-hour LC^« value for Coho salmon at 325
ppm. Hiltibran (1967) stated that bluegill, green sunfish, lake
chubsuckers, and small-mouth bass fry were able to tolerate 50 ppm
aminotriazole for 8 days with no observable adverse effects.
Lower Aquatic Organisms
An EPA report by Newton and Norgren (1977) said that Daphnia were
"very sensitive" to aminotriazole, and the 48-hr LCj.« value was given
as 3 ppm. On the other hand, Crosby and Tucker (1966) cited the
median immobilization concentration for D. magna as 23 ppm.
Bees
Aminotriazole may be slightly toxic to bees. The effect of dusting bees
with 12.09 ug/bee produced a 5% mortality in a study by Atkins et al.
(1973), Field doses of 1 kg /ha would equal 12 ug/bee.
Soil Microorganisms
A study by Fletcher (1960) concluded that when aminotriazole was
applied at recommended rates of 8, 4, 2 and 1 lb /acre, the rate of
nitrification was depressed and the number of microorganisms was
reduced. A study by Ludzack and Mandia (1962) showed that
aminotriazole inhibited microbial respiration and nitrification of activated
sludge. Chandra (1964) showed a decrease of nitrifying bacteria in
soil. Grossband and Wingfield (1978) showed that the decomposition of
cellulose by fungi was reduced when high amounts (500 ppm) of
aminotriazole were present in soil samples.
Bioaccumulation
Studies by MuUison (1979) and Newton (1979) stated that
bioaccumulation was not of major concern because of aminotriazole' s high
solubility in water and its insolubility in cellular lipids. However, no
data are available on the subject.
11-14
B. AMMATE
1. INTRODUCTION
®
Ammate is the trade name for an inorganic herbicide, ammonium
sulfamate, mani.factured by E. I. du Pont de Nemours and Company.
®
It is also called AMS, Amcide , and Ai
has the chemical structure shown below.
® ® /
It is also called AMS, Amcide , and Ammate X (Thomson, 1977). It
0
II
KN-S-0-NK
2 II ^
0
Relevant physical and chemical properties are presented below in the
discussion of the fate of ammonium sulfamate in soil.
2. TOXICITY
Acute Toxicity
Acute oral toxicity studies show a low order of toxicity for ammonium
sulfamate. The acute oral LD^. for ammonium sulfamate is 3900 mg/kg
for rats (Du Pont, 1972b) and 5760 mg/kg for mice (Maki, 1973). When
administered subcutaneously , the LD_- is 1438 mg/kg (Maki, 1973). No
symptoms of irritation or systemic toxicity were noted from repeated
applications of 20% or 50% aqueous solutions to the shaved skin of rats
(Du Pont, 1972a). Likewise, no adverse reactions were observed in a
test by Aoyama (1975) after ammonium sulfamate was administered to the
skin of rats.
Subacute /Subchronic Toxicity
Du Pont (1972a) fed rats 10,000 ppm for 105 days and found no clinical
signs of toxicity or pathology. Dietary administration of 100, 250, and
11-15
500 mg/1 to rats for 90 days resulted in no effects on appearance,
behavior, survival, or relative organ weights. At the highest dosage,
body weights were reduced (Gupta et al., 1979).
Special Studies
There is very little information on the long-term toxicity of ammonium
sulfamate. No indications of adverse toxicologiceil effects (including
effects on reproduction and lactation) were found by Sherman and Stula
(1965) after administration of ammonium sulfamate in the diet of male
and female rats for 19 months at dietary concentrations of 350 or 500
ppm. Although it is not clear whether tissues were examined
microscopically for tumor induction, this study also suggests a lack of
carcinogenic effect.
Negative results were noted for ammonium sulfamate (5 ul/ plate) in an
Ames/ Salmonella assay (Anderson et al. , 1972).
Summary
An evaluation of important toxicity data is provided at the end of this
chapter.
3. MOBILITY AND PERSISTENCE
Fate in Soil and Water
Limited information is available on the environmental fate of ammonium
sulfamate. Thomson (1975) states that ammonium sulfamate "breaks
down rapidly in soil in the presence of moisture and high temperature."
EPA (1981a) reviewed the data submitted for registration of ammonium
sulfamate in a pesticide registration standard review in 1981. They
stated that "the submitted data are insufficient to predict the fate of
ammonium sulfamate (AMS) in the environment." The only study which
EPA considered scientifically valid was done by Konnai et al. (1974),
which showed that ammate is "very mobile" in the soil and exhibits a
distribution parallel to mass flow. In this study, ammonium sulfamate
(95% powder) was applied to an unspecified soil at high rates (50
kg/ha). After application of 2 cm and 50 cm of water, the ammonium
sulfamate moved 14 cm and 50 cm, respectively.
11-16
Movement of ammonium sulfamate in the soil is suggested by its high
water solubility, which is 216 g/100 ml at ZS^C (Oullette and King,
1977) for the technical material. One formulation, AMMATE-X-N Weed
and Brush Killer, has a somewhat lower, but still high, solubility of 68
g/100 ml water (Du Pont, 1972b). Ammonium sulfamate is considered
non-volatile (Thomson, 1975, no data provided). At normal tempera-
tures and pH, the hydrolysis rate is considered negligible (Du Pont,
1972a).
Indicators of Potential Ground Water Contamination
Table II-4 provides information on parameters associated with the
mobility of ammate. These parameters, and their associated thresholds,
have been suggested by EPA for use in assessing the potential for
pesticide contamination of ground water. A discussion of these param-
eters and thresholds, and the methods for arriving at designated values
for individual herbicides , is presented in the main body of the report
as part of the discussion of the fate of herbicides in the environment.
TABLE II-4
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
AMMATE
Indicator
Solubility
Value for Ammate
Threshold
K
DC
Speciation at pH 5
Hydrolysis half-life
Photolysis half-life
Vapor pressure
2,160,000 ppm
at 25°C
>30 ppm
ND*
<300-500
Neutral (anionic
Anionic
and cationic charges
cancel out)
(negatively
ND*
>6 months
ND*
>3 days
Non-volatile
<10 mm Hg
* ND = no data.
11-17
4. TOXICITY TO NON-TARGET ORGANISMS
Birds and Fish
Avcdlable data suggest that ammonium sulfamate is non-toxic to birds
and fish. For quail, the LD^q is 3000 mg/kg (Maki, 1973). The 24-hr
TL and 96-hr TL for channel catfish were found to be 259 ppm and
mm ^^
203 ppm, respectively, in a study by Clemens and Sneed (1959). A
study by Alabaster (1969) found a range of 55 ppm to 3200 ppm for the
LC-j^ for harlequin fish. Curtis and Ward (1981) found no significant
mortality in fathead minnows when they were exposed to 600 mg/1 of
ammonium sxilfamate for 96 hours.
Mammalian Wildlife
A study by Haugen (1953) indicated no signs of illness when deer were
fed either crystals of ammonium sulfamate or foliage of various trees
treated with ammonium sulfamate. The amount of herbicide consumed
was not determined.
Soil Microorganisms
Thomson (1975) states that ammonium sulfamate "may cause temporary
soil sterility." On the other hand, ammonium sulfamate was found to
alleviate the inhibition of fungal growth caused by carbaryl (Cowley and
Lichtens tein , 1970).
Toxicity Data Evaluation
Insufficient information is available to assess the carcinogenic, tera-
togenic, or mutagenic potential of ammonium sulfamate. EPA's registra-
tion standard pointed out these inadequacies as well as insufficiencies in
the data regarding eye irritation, acute oral toxicity, acute dermal
toxicity, subchronic oral toxicity, and subchronic dermal toxicity. No
studies in EPA's registration files on ammonium sulfamate were con-
ducted by IBT.
11-18
C. ATRAZINE
1. INTRODUCTION
Atrazine is the common name of the herbicide 2-chloro-4-ethylamino-
6-isopropylamino-s-triazine. It is produced by Ciba-Geigy and is
marketed under the trade name AAtrex. Combinations of atrazine with
®
other herbicides include Bicep 4.5L (atrazine and metolachlor) , Atratol
SOW (atrazine and prometon), Atratol 8P (atrazine, sodium chlorate,
®
and sodium metaborate) , and AAtram 80G (atrazine and propachlor) .
The structure of atrazine is:
H ^N
{CH3)2CHN^^^
N
N
HNCH2CH3
Relevant physical and chemical properties are described below in the
discussion of the fate of atrazine in soil and water.
2. TOXICITY
Acute Toxicity
Acute oral toxicity studies show a low order of toxicity for atrazine.
Oral LDg.^ values, summarized in Table II-5 range from 750 mg/kg to
3080 mg/kg for rats, mice, rabbits, and hamsters. Lewis and Tatken
(1980) reports a dermal LD^q value of 7500 mg/kg. When 38 mg of
atrazine is applied to the skin of a rabbit, a mild irritation results.
Application of 6.32 mg to rabbit eyes (standard test for eye irritation)
results in a severe reaction.
11-19
TABLE II-5
ACUTE ORAL TOXICITY OF ATRAZINE
(LD^Q, mg/kg)
Form
Rats
Mice
Rabbits
Atrazine
3080
3080
3800
1750
1750
1750
750
Hamsters Source
Thomson (1975)
Ouellette and King (1977)
MuUison (1977)
1000 Lewis and Tatken (1982)
Subacute Oral Toxicity
On the basis of a limited number of reports, atrazine does not cause
any observable adverse effects when fed to cattle, dogs, and horses.
In one subacute toxicity study, atrazine in an 80% wettable powder form
was fed to cows at either 100 ppm for 21 days or 30 ppm for 4 weeks.
In each case, no ill effects were observed (Ciba-Geigy, 1971). One
report states that in studies in which 25 ppm atrazine was fed to dogs,
cattle, and horses for extended periods of time, no ill effects were
observed (MuUison, 1979).
Mammalian Metabolism
In rats given radiolabeled atrazine, 85% was excreted in urine and feces
after 72 hours. The remaining radioactivity was found in the lung,
liver, and kidney, with lower concentrations in muscle and fat. The
most common metabolic reactions are dealkylation of the amino group ,
hydrolysis of the 2-chloro-group , and oxidation of an N-alkyl side-chain
to carboxylic acid and alcohol (Erickson et al. , 1979) .
Special Studies
Carcinogenicity Only one study was available regarding the
carcinogenicity of atrazine. This study suggests that atrazine is not
carcinogenic in mice. Male and female mice (C57BL/6 x C3H/Anf) and
(C57BL/6 X AKR) were given 21.5 mg/kg by gavage from days 7 to 28
of age, followed by a dietary dosage of 82 ppm for approximately 18
11-20
months. No increase in incidence of tumors above control values was
noted (Innes et al. , 1969).
Teratogenicity / Reproduction No teratogenic effects were observed in a
study by the U.S. Department of Health, Education, and Welfare
(1969). Atrazine was administered subcutaneously to mice at a level of
46.4 mg/kg (in 0.1 ml dimethyl sulfoxide) from days 6 to 14 of
gestation. No significant increase in malformations was observed among
the offspring of treated mothers.
Reproduction In a series of experiments, Peters and Cook (1973)
examined the effects of atrazine on reproduction in rats. No effect on
the number of pups /litter or weaning weight was seen in the offspring
of rats fed up to 1000 ppm atrazine in the diet throughout gestation.
Subcutaneous injections of up to 200 mg atrazine/kg of days 3, 6, and
9 of gestation had no effect on the number of pups per litter. No
indications are provided on whether any other parameters were
monitored.
Subcutaneous injections of higher doses (800-2000 mg/kg) under the
same test conditions were embryotoxic. One of the seven rats injected
with 1000 mg atrazine/kg had a normal litter; all embryos were resorbed
in the six other dams in this treatment group and in the group given
2000 mg/kg. One of four dams in the 800 mg/kg groups had no pups.
(It is unclear from the data presented whether the authors looked for
resorptions and found none, or did not monitor this effect in this
group.) Although the authors did not report maternal toxicity, it
appears highly likely that maternal toxicity did occur above 800 mg/kg.
Atrazine is moderately toxic to rats when administered by injection.
The lowest reported lethal dose by injection (intraperitoneal) for this
species is 550 mg/kg (Lewis and Tatken, 1982). The embryotoxicity
noted at levels above 800 mg/kg may therefore be an indirect response
to toxic effects in the dams.
Using the egg injection technique, Dunachie and Fletcher (1970) noted a
decrease (27%) in hatching in chick eggs injected with 400 ppm atrazine
11-21
(in 90% methanol). No effect was observed at 300 ppm. It should be noted
that a great deal of variability in the percentage hatching was observed,
and no clear dose response was evident for einy of the tested herbicides.
Mutagenicity As shown in Table II-6, most of the available studies indicate
that atrazine is not mutagenic. The data suggest that activation by plant
enzymes is required to produce a mutagenic response, and that mammalian
liver enzymes appear incapable of activation.
Other Information Bontoyan et al. (1979) screened a variety of technical
and commercial pesticide formulations for the presence of nitrosamine con-
taminaaits. Negative findings were reported for atrazine. The limit of
detection, however, was only 1 ppm.
Summary An evaluation of important toxicity data is provided at the end of
this chapter.
3. MOBILITY AND PERSISTENCE
Fate in Soil
Atrazine is generally considered to have limited mobility (Newton and Nor-
gren, 1977; Schlapfer, 1977; Kozlowski and Kuntz , 1973), and it is readily
adsorbed onto soil particles (Von Rumker et cil., 1975; Witt and Baumgart-
ner, 1979) . Koslowski and Kuntz (1973) report that leaching of atrazine is
also insignificant in sand, based upon a study of atrazine which was applied
to Plainfield sand at rates of 1, 2, 4 lb /acre. When 2, 4, and 8 inches of
water were used, most of the atrazine remained in the first inch of soil.
The application of additional water resulted in the leaching of a portion of
the atrazine downward to a depth of 6 inches. Similar results were
obtained by Marriage et al. (1975). When atrazine was applied to plots of
sandy loam soil at a rate of 4.5 kg /ha for 9 consecutive years, the herbi-
cide remained in the upper 15 cm of soil, and the majority of that was in
the 0-5 cm soil layer. The maximum residue level was measured as 0.4
kg/ha in the top 15 cm of soil. In a loam soil to which 2-20 lb a. i. /acre
atrazine was applied and which received 8.16 inches of rainfall, 85.3% of the
applied atrazine was found in the top 1 inch and 5.7% was found in the 1-2
inch layer, after one year (Birk and Roadhouse, 1962).
11-22
0)
u
o
<N3
fM
00
OO
(T-
O^
(0
(TJ
■<->
•*-»
V
0)
•fj
-M
4)
o;
1—1
1— 1
l-H
0
o
^
X
U
U
o
00
pH
^
>-^
(A
rtJ
•
I— 1
2
a
s
T)
2
^
u
u
h
<tf
13
N
:s
OO r-
1— t o^
^ 2
I— I ^
(U «3 c
< o s
o
00
u
1—1
T3
<
o
00
o
u
o
u
vO
1
<
z
1-4
Pi
H
<
c/2
H
W
H
H
t— I
O
z
O
<
H
D
IS
en
+->
C
<u
6
S
o
U
3
en
0)
}h
»4
i-H
0)
0)
en
tn
N
o
15
130
E
>^
N
C
0)
E
c
•t-»
o\o
O
•
o
■M
•1-4
C CO
>
f— 1
00
m
-0 ^
•
•
•
•
r2
@
15
•r-<
c ^
c ^
•i-i
• fH
o
<U
+
+
00
<0
• IH
• f-H
bO
!30
^-1
1 ppm
for 7
r~
^
^
bO
00
X
1 pptr
for
S
E
bO
CM
0)
-4->
<
<
E
o
rH
>
U
13
TJ
a
0)
T3
^3
'O
TS
nJ
rtJ
U
en
en
X
E
E
en
>>
>N
U
N
N
O
c
C
M-l
(U
(U
2
u
4-)
(U
c
■vf'
>
cti
1
• 1-H
p— <
o
E^
pH (V) ^_J (l4 .-H
CO
CM
I
I I +
+ I +
E
en
>^
W
■♦-»
en
0)
^ C
C
•r-l
E
o
4}
en
o
2
(0
u
•t-l
■*-»
c
bO
" o
CiO
p— I ra
E £
E <u
c en
en
en
o
2
o
u
03
0)
C
O
en
o
0}
c
o
bO
o
-M
03
E
u
a
en
<u
en
o
o
!h
OS
E
0)
c
o
<u
en
O
o
u
u
03
E
<u
C
o
en
o
2
o
u
u
03
C
o
D
en
:3
o
C3
•♦J
03
c
.1-1
E
o
T3
03
03
^^
r— (
'r^
.pH
rC
-C
a
a
o
0
en
en
0
0
^
U
Q
Q
u
• pH
CO
■4-J
1—1
0)
13 en
C
y S
0)
(U
bc
>s U
o
;->
+->
03 <^
>>
> "^
u
0>
a
U ^H
03
« <u
■4-» +-<
03
en en
E
E E
E
03
03 03
rC Xi
E
(U <u
en en
0
<U 0)
c c
• rl .i-H
>
pC x:
u u
C
(0
1—1
<0
u
o
E
•l-t
u
en
u
•i-i
u
u
o
C/3
o
00
o
00
p— 1
l—i
■ — '
<u
F-^
^ (T3
^»-v
1-^
o <u
o
oo 2
c»
-M
o^
CT^
ID
,-H -^
rH
"^ c
^^
0
;. «»
^H
a
•U .LJ
0)
o
1—1 +j
r— 1
(J
'5*0
TJ
a
< c/^
<
CSl
o
00
o
(0
<u
o
00
o
00
00
rt
(U =
•^.^
0
■..^
s.^-
0
•M
u
u
^
^
V4
a
^
1)
(U
(U
o
P3
l-H
1— t
fj
^
(U
T3
13
<
TJ
<
<
ISl
CM
00
flj
o
00
0)
1— 1
•M
v^
1-^
u
1— 1
0
1— 1
^
-a
U
<
W
2
1— 1
l>3
^-^
<
Q
p:J
w
H
p
<
2
KH
H
• V
2
O
O
CO
H
H
1
>^
t— 1
1— 1
H
HH
W
o
J
1— 1
CQ
2
<
O
H
CO
c
E
E
o
U
tn
CO
l-H
1—1
E
N
E
>>
c
;4
C
0
0)
QJ
&£
V4
c
OJ
X
>
■**^
00
bO
•ft
'a
E
piti
•~~-
+
+
o
o
r— 1
£
&0
,i«i
GO
1
1— H
o
^**^
*■*-*
o
03
o
00
IHO
o
U
o
t— t
o
r—^
f— 1
rH
3
a;
t:
(U
T3
'O
rt
T3
^3
en
TJ
-a
(U
U5
(U
0)
E
(U
(U
^3
^
-0
T3
13
T3
^
T3
>>
-a
^3
rJ
-^
rt
ra
03
en
w
(U
Ul
cn
(U
U
V
0)
(U
E
^
E
C
E
E
N
E
0-
N
I— H
N
^9
C
c
a
c
C
<u
V
(U
(U
a
• ««
+->
-t-J
2
E
-M
u
c
o
c
C
(U
nJ
o
fiS
05
>
1— t
o
l-H
•ft
P^
00
s
sO
0^
J
2
E
CO
-a
Ri
(Q
0)
B
>>
c
a
n5
2
E
+ +
(U
^
a
u
^
o
a
R>
CO
CO
CO
'o
en
^
1—4
•rH
o
•11
1— t
u
iated ai
. coli
r— 1
§
•♦->
o
o
CO
£
0
u
03
o
E
s
l-H
OS
CO
03
CO
:3
>>
(fl
73 W
m
>>
S
E
o
03
0) -~~
**»...»
"*•■»»
•11
to
3
CO
:3
0)
o
cn
o
N
• ii
(fl
to 0
o
o
9-
^
(U
o :2
12
2
CO
■M
<J
H
X
<:
cn
cn
05
•i-t
tn
•11
>
u
u
cn
a;
o
£
o
05
X
o
u
OS
C/3
o
nO
00
r-
a>
O^'
o
oo
a
0
<u
u
u
(4
u
u
0
u
o
rt
w
M
(4
(U
<U = --H s
ID
O
pa
(U
-a
•4-»
o
c
QN I— t
«5 ^ 00
<
^ oo
0)
C
o
en
u
<
<u =
o
u
o
o
CO
T3
C
I— H
01
a
o
o
00
01
•4->
0)
cn
01
CQ
(tf
CO
C/3
Q
w
o
2
I— I
H
2
O
U
I
CQ
<
2
I— «
<
H
I— I
o
1—1
2
o
<
H
D
en
• •
C/3
H
E
C/2
S
0
U
3
01
pei
<U
73
T3
nJ
(0
0)
E
CSJ
C
>
t3
01
en
<u
E
>^
N
c
c
01
J cu
^
j:
o
E
a
Du
o
o
o
en
u
o
E
a
o
o
o
0)
C
•>M
N
01
U
o "*
S
w Du
"^ IT)
I
O
J3
3
cn
tn
o
o.
rt cfl ^
^ E (U
cn
E
M
C
0)
>
01
(0
lU
E
c
<u
a;
>
+
-t-"
01
'a
3.
o
o
I I
T3
(U
TO
T3
01
(n
S
c
>
(U
TJ
01
cn
E
c
c
01
3
o
cn
•2 flJ
o >
01 w
0)
cn 73
cn -M
•♦-> 01
cn il
o
01
■*->
X
;3
0)
c
• rH
M
01
U
+->
01
01
cn
o
o
C
o
00
cn "^
ol u
"^ DO
< ^
01
.S a
03
■M +j :;5
cn -tr o
^-^ ? cn
in
I
cn
D
s
>>
•*-»
E
cn
0
!>>
u
W
ol
^
•*->
u
cn
o
<u
03
H
m
I— I
c
o
_S
Id
CO
E
<
cn
cn
cn
•f-i
(J
ol
pa
01
cn
cn
01
o
pEi
i-H 00
u
o
n)
0)
03
3
(U
en
Cti
^
^
(U
•(-4
I— 1
X
-a
m
<
OJ
o
en
(U
C
<
u
o
o
04
i
Q
W
2
I— t
H
2
O
O
1
<
W
2
I— I
<
<
H
w
H
H
l-H
o
2
W
o
<
H
D
IS
en
c
E
a
o
U
3
en
DO
3.
O
CO
<
1—4
O
u
en
>>
W
^H
(U
4J
Xi
cn
o
<u
cn
H
W
O &0
tn ^
3
s
$1
V4
4)
I— <
a
C
o
c
o
OJ
a.
Other studies have shown higher mobility. In one study in which
atrazine was applied at concentrations of 0.5-2 ppm to a Sharpsburg
silty clay loam soil, atrazine residues (amount not given) moved to a
depth of 90 cm (ca. 36 inches) and remained there for after 41 months
(Lavy et al. , 1963). Residues at shallower depths dissipated during
that time. Similar results were found by Harris et al. (1970), who
found that atrazine moved to a depth of 38 cm (15 inches) and
persisted longer at these lower depths. Atrazine was applied to three
sandy loam soils in Nevada and Idaho at rates of 1.2 to 9.6 lb a. i. /acre
atrazine. After 1 year, residues in the top 6 inches of soil ranged
from 0.005 ppm to 0.25 ppm. In the next 6 inches of soil (6-12 inches
below the surface) residues ranged from 0.05 ppm to 0.15 ppm (EPA,
no publication date provided [a]).
A number of factors have been found to influence the mobility of
atrazine by influencing the amount of atrazine that is adsorbed.
Adsorption is greater at lower temperatures, at lower pH, under dryer
conditions, and, especially, in soils with higher percentages of organic
matter (TRW, 1981).
Several field studies have been done to determine the potential for
surface water contamination from runoff containing atrazine. Von
Rumker et al. (1975) suggests that the potential for high concentrations
of atrazine in runoff water is significant, especially if rainfall occurs in
the first 2 weeks after application.
Triplett et al. (1978) studied the runoff after atrazine had been applied
to several watersheds ranging from 0.4 to 3.5 ha in area. The highest
concentration of atrazine detected was 0.48 ppm, which occurred soon
after application.
Atrazine is generally considered a persistent herbicide. A review
article by Sheets (1970) suggests that in agricultural soils, residues
often persist at phytotoxic levels for greater than 1 year. Several
studies (Buchanon and Hiltbald, 1973; Ritter et al. , 1974; and Best et
al. , 1975) suggest that atrazine can persist 1 to 2 years. The data
11-27
presented above regarding the mobility of atrazine substantiates its
persistence, since in all of the studies samples were taken after a year
or more. One study mentioned above in regard to mobility suggests a
particularly long persistence. In a loam soil that received 2-20 a.i./lb
acre atrazine and 8.16 inches of rainfall, a total of 91% of the applied
atrazine remained after 1 year in the top 2 inches of soil.
Although the amount of loss by volatilization is not fully understood,
this route of loss is generally considered to be insignificant because of
-8 °
atrazine' s low vapor pressure (ranging from 5.7 x 10 at 10 C, to 2.3
-5 °
X 10 at 50 C) (TRW, 1981). Volatilization of atrazine occurs generally
in the first 2 days after application (MuUison, 1979; Hammons, 1977).
Loss by photodecomposition can be significant if residues are subjected
to high temperatures and prolonged sunlight before precipitation.
Photodecomposition would probably not be significant, therefore, on
shaded soil (TRW, 1981).
Although atrazine is considered to be a stable compound, chemical and
microbial degradation are known to occur and have been studied exten-
sively. Chemical degradation of atrazine by a first-order hydrolysis
reaction has been observed to occur in soil (Zimdahl, 1970; Armstrong
et al. , 1967). The rate of hydrolysis is a function of pH and is base
and acid catalyzed such that at pH values of 2.2, 3.1, 11.1, and 11.9,
the half-lives of atrazine are 18.4, 66.4, 81.1 and 15.2 days,
respectively.
Two studies (EPA, no publication date provided [a]; Kearney et al. ,
1977) proposed that nitrosoatrazines may be formed if NaNO_ is present
in concentrations of 100 ppm (as N) or greater and at pH values of 3
or less. However, since these conditions rarely occur, the formation of
such compounds should be insignificant in natural soil systems.
Microbial decomposition occurs by three routes, dealkylation , ring
cleavage, and the hydroxylation of the 2-chloro group (TRW, 1981).
Dealkylation is believed to be the primary mechanism and was observed
to occur in the presence of 12 different types of fungi, 2 of which were
11-28
Rhizopus stolonifer and Aspergillus fumigatus (Kaufman and Blake,
1970). Ring-cleavage reactions were studied by Roeth et al. (1969) and
by McCormick and Hiltbold (1966). Both showed that microbial cultures
degraded the atrazine to hydroxy-atrazine by a ring cleavage. Further
degradation of the hydroxy-atrazine was found to be three times faster
than degradation of the parent compound in a mixed microbial
population. These secondary reations give rise to metabolites which
may be subject to further degradation (Kearney and Kaufman, 1975;
Ramsteiner et al. , 1972).
Fate in Water
There have been very few studies concerned with the fate of atrazine
in water. Klaasen and Kadoum (1979) studied the distribution and
decay of atrazine that had been applied at an initial concentration of
0.3 ppm to a farm pond. The atrazine appeared to be persistent in the
water and the mud. The concentrations measured at days 1 and 120
decreased from 309 to 206 ppb in the water and from 323 to 204 ppb in
the mud. In a 1975 study (EPA, no publication date provided [a]) of
seven major rivers in the central United States, peak residues occurred
during the months of heaviest application (May to June). After June,
the residual levels were S 1 ppb . The maximum concentration of
atrazine detected was 16.7 ppb.
Photodecomposition of atrazine probably does not occur to any signifi-
cant extent in water, due to its extremely slow reaction rate (Wolfe et
al. , 1976) . It has been shown in the laboratory that photolysis of
aqueous atrazine yields 2-hydroxy-atrazine. Laboratory photolysis of
aqueous atrazine with ultraviolet radiation at 253.7 nm yields a
2-hydroxy compound. This is probably due to the nucleophilic
displacement of the chlorine atom (Wolfe et al. , 1976).
Indicators of Potential Ground Water Contamination
Table II-7 provides information on parameters associated with the
mobility of atrazine. These parameters, and their associated thresholds,
have been suggested by EPA for use in assessing the potential for
pesticide contamination of ground water. A discussion of these
11-29
parameters and thresholds, and the methods for arriving at designated
values for individual herbicides, is presented in the main body of the
report as part of the discussion of the fate of herbicides in the
environment.
TABLE II-7
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
ATRAZINE
Indicator
Solubility
K
oc
Speciation at pH 5
Hydrolysis half-life
Photolysis half-life
Vapor pressure
Value for Atrazine
33 ppm at 27°C
81.6
Neutral or catonic
42 days (pH 5)
>14 days
(natural light)
3.0 X lo"^ mm Hg
at 20°C
Threshold
>30' ppm
<300-500
Anionic
(negatively charged)
>6 months
>3 days
-2
<10 mm Hg
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Atrazine appears to be non-toxic to test birds. Heath et al. (1972) and
Hill et al. (1975) reported LC... values from a 5-day diet to be greater
than 5000 ppm for bobwhite quail, Japanese quail, ring-necked
pheasants, and mallard ducks. Tucker and Crabtree (1970) reported
an LDp.- for mallard ducks to be greater than 2000 mg/kg. Studies by
Mullison (1979) and by Heath et al. (1972) reported LD values for
mallards and pheasants to be greater than 5000 ppm, and for bobwhite
quail, 700-800 ppm.
11-30
Fish
Available data suggest that atrazine is toxic to some species of fish.
Toxicity data are summarized in Table II-8. Studies by Mullison
(1979), and by Newton and Norgren (1977) showed that goldfish and
bluegill sunfish had 48-hr LC ^ values of 118 mg/1; Butler (1965)
showed that rainbow trout had a 48-hr LC_- of 4.5 mg/1. The authors
concluded that atrazine had a low toxicity to goldfish and bluegill, but
was toxic to rainbow trout.
Vivier and Nisbet (1965) used atrazine in the form of A361 and found
that 0.5 ppm of A361 was lethal to 20% of a minnow population in 72
hours. The TL for minnows was 1.25 ppm. When atrazine in the
m
form of Gasaprime was used, the 24-hr and 48-hr TL values for
'^ m
minnow were 3.75 and 2.5 ppm respectively. Jones (1962) found a
survival rate of 90% for 72 -hour exposures for Micropterus salmoides fry
at 5.0 ppm, Letalurus puctatus at 10.0 ppm, and Lepomis macrochirus
at 10.0 ppm. A review study by EPA (no publication date given [a])
noted a 20%-30% reduction in the growth of a variety of fishes
(including gizzard shad, channel catfish, bluegill sunfish) when treated
with 500 ug of atrazine per liter of water. The number of offspring
was reduced by 96% at both 20 and 500 yg/l.
Lower Aquatic Organisms
In field studies by Walker (1964), atrazine was applied to ponds at
concentrations of 0.2 to 6.0 ppm. The author concluded that atrazine
was somewhat toxic to bottom fauna. Mayflies, caddis flies, leeches,
and gastropods were among the most sensitive species. The bottom
fauna appeared to recover in 4 to 6 months after treatment. Walker
(1962) applied 0.5-2.0 ppm of atrazine to ponds and found that clams
were reduced to 1/8 of their original number, while the snail population
increased four-fold. Fingernail clams, isopods, and damselflies showed
no mortality when subjected to 20 ug/1 and 500 yg/l of atrazine in an
EPA study (publication date not given [a]). Additional data is
summarized in Table II-9.
11-31
0)
o
u
o
^^
r-
r-
ir>
r-
r^
sO
o^
a^
o^
(— (
1—1
.-1
C
C
0)
(U
4)
/■"v
o
,^
0
O^
2
o
2
2
-a
T3
T3
C
C
o^
C
=
(TJ
01
1— 1
rt
c
C
^^
^
o
CO
o
0
en
O
<u
•i-t
•4->
•f^
4->
•IH
>
•l-t
^
r—l
^
9
(U
3
<u
S
>
2
2
:2
2
«
00
I
<
O
H
2
I— I
M
<
H
<
O
H
H- 1
u
l-H
X
o
a
;3
en
0)
pel
03
in
CM
in
CO
in
00
00
E
E
E
o
in
o
in
J
J
J
U
U
H
H
H
J
h:i
V4
Sh
h
;^
u
1
1
1
1
43
1
1
00
1
1
oo
1
00
1
00
"^
(NJ
Xl^
'sr
•«*
in
O
in
U
E
a
■*->
o
0)
o
2
o
in
O
I
00
^_
^
^
J2
en
^
^
^
•l-l
(0
o
CO
0
0
o
OD
c«
-Q +j
o
c
c
c
<u
T3
C 3
•«-»
<u
c
c
c
3
r- H
•S 0
o
CL
<F^
•^H
•IM
1—1
0
0.
C/3
2
2
s
CQ
a
CO
c
o
a>
■4->
E
05
• r<
(— ^
^
;3
1—1
03
E
vO
a
Jh
CO
en
0
03
fa
<
u
C
01
S3
•iH
u
9i
•IH
a
u
C
•1-1
OJ
U
Indirect Effects on Aquatic Ecosystems
A review study by EPA (publication date not given [a]) found that
small ponds exposed to small amounts (20 and 150 yg/1) of atrazine for
135 days showed an immediate decline in the rate of photosynthesis by
aquatic algae. Within a few weeks, the growth of atrazine-resistant
plant species increased. Zooplankton reproduction rates (Simocephalus
and Daphnia) were reduced by 57% and 70% respectively with 500 ug/1,
and by 9% and 70% respectively with 20 ug/1. By day 15, the
zooplankton biomass was reduced by as much as 60% with both 20 ug/1
and 500 ug/l» and the species composition was affected by both
concentrations of atrazine.
Effect on Livestock
MuUison (1979) reported that cattle, dogs, and horses fed a diet of 25
ppm atrazine over an extended period of time produced no observable
adverse effects. Palmer and Radeleff (1969) reported the toxic dosage
of atrazine for cattle to be 25 mg/kg after 8 doses by drench and 2
doses by capsule. Chickens given 10 doses at 50 mg/kg had significant
reductions in weight gain. The toxic dosage for sheep was 5 mg/kg,
although it appeared that some sheep may be less sensitive than the
average.
Bees
No data was found on the effect of atrazine by itself on bees. However
one study by Sonnet (1979) that studied the synergistic effect of
atrazine with insecticides showed no significant mortality when bees
were fed sublethal doses of insecticides plus atrazine, as compared to
being fed only insecticides.
Bioaccumulation
The limited data available suggests that atrazine may concentrate to a
limited extent in a number of organisms. In data provided by the EPA
(publication date not given [a]) maximum residues in fish were
estimated at 500 ppb when the concentration in the water was 16.7 ppb.
At a near-normal concentration of 1.0 ppb in water, the concentration
in fish was 20 ppb. After treatment of a model aquatic ecosystem with
11-33
TABLE II-9
TOXICITY OF ATRAZINE TO LOWER AQUATIC ANIMALS
Species
Shore crab
Cockle
Brown shrimp
Oyster
Shrimp
Test
LC
50
96-hr EC
48 -hr EC
50
50
Result
>100 ppm
>100 ppm
10-30 ppm
No effect at
1.0 ppm
30% at 1.0 ppm
Source
Portman and Wilson (1971)
Butler (1965)
0.82 ppm atrazine (in bottom soil), Kearney et al. (1977) found bioac-
cumulation ratios in algae, fish, and snails to be 9, 16, and 8, respec-
tively. Percich and Lockwood (1978) have done a study indicating that
atrazine accumulates in some species of fungi.
Soil Microorganisms
Studies of atrazine' s effect on soil microorganisms seem to produce
varying results. A study by Percich and Lockwood (1978) showed
atrazine to be a growth stimulant to microflora when Conover loam soil
was treated with 10, 30, and lOOmg/g. Studies done in the Soviet
Union by Kozlova et al. (1967), Milkowska and Gorzelak (1966), and
Sosnovskaya and Pashchenko (1965) confirmed these data.
In comparative studies done by Volts et al. (1974), it was shown that
atrazine applied at a rate of 4 kg /ha reduced populations of anaerobic
bacteria, sporeformers, cellulolytic microorganisms, and nitrifying,
amylolytic, and denitrifying microbial groups.
Toxicity Data Evaluation
Insufficient information is available regarding the carcinogenicity and
teratogenicity of atrazine. In regard to carcinogenicity, relevant tests
have recently been submitted by the manufacturer to EPA for review,
and EPA has reviewed one of these studies. Although no statement has
been issued by EPA, it can be reasonably assumed that this test did
11-34
not show positive effect, since no "rebuttable presumption against
registration" resulted from this review. A similar statement can be
made for the rodent teratogenicity test, which has been recently sub-
mitted to and accepted by EPA.
While it is never possible to say that no further study is needed, the
data base regarding mutugenicity for atrazine is sufficient to draw the
conclusion stated several paragraphs above. The testing of mutagenic
potential is an inexact science — some false positive or false negative
studies are to be expected. In regard to atrazine, only eight of the 47
studies conducted show positive findings without activation by plant
enzymes. Given the extensive amount of study this subject has already
received, a judgement must be made on the basis of the majority of
results. In regard to the possibility of activation independent of the
liver, mentioned by the Conservation Law Foundation in its review of
the draft GEIR, our review concluded that insufficient data were pro-
vided by Adler (1980) to justify his suggestion of this possibility.
The registration standard for atrazine cites the need for a non-rodent
teratogenicity study, a gene mutation, and a gene metabolism study,
and an update of the reproduction study currently on file in order to
satisfy recent protocol guidelines. (Other deficiencies which are not
related to mammalian toxicology include data on hydrolysis, photode-
gradation in soil, metabolism in soil and water, leaching potential, soil
degradation, and accumulation in crops, fish, and lower aquatic organ-
isms.)
Two chronic oral studies in EPA registration files were conducted by
IBT. Portions of both of them were found to be valid, and EPA has
decided both can be used for supplemental information. One study has
been replaced by Ciba-Geigy; no response has yet been made regarding
the replacement of the other study. Other chronic oral studies on
atrazine in EPA files have been conducted by other laboratories.
11-34. 1
D. BROMACIL
1. INTRODUCTION
Bromacil is the common name for the herbicide 5-bromo-3-sec-butyl-6-
methyl uracil, produced by E. I. du Pont de Nemours and Company.
® ® ®
Its formulations are known as Hyvar , Hyvar-XL , Hyvar- XP ,
Nalkil , Urox B , Urox-HX , Ureabor , Boracil , Borea , Hibor ,
® ® ® /
Instemul , Bro-40 , and Uragen (Thomson, 1975; Ouellette and King,
1977; EPA 1980a). Bromacil is a substituted uracil compound with the
following structure:
H
C
I
CH
N-C-CH2CH3
3
Relevant physical and chemical parameters are presented below in the
discussion of the fate of bromacil in soil and water.
2. TOXICITY
Acute Toxicity
Bromacil appears to have a low acute toxicity. Ouellette and King
(1977) and Thomson (1975) list the oral LDrn value of bromacil to
laboratory animals as 5200 mg/kg. A technical data sheet reports the
acute oral LD-,. for dogs to be greater than 5000 mg/kg. With dermal
application, the acute lethal dose was found to be greater than 5000
mg/1 (maximum feasible dose). No toxic symptoms were observed at
this dose (Du Pont, 1979a). The inhalation LCj.-. for rats is greater
than 4.8 mg/1, using an 80% formulation (Du Pont, 1979a).
11-35
Bromacil appears to be moderately irritating to the skin when applied as
a 50% aqueous suspension (80% WP) to intact or abraded skin of guinea
pigs. No skin sensitization occurred. A slight transient conjuctival
irritation of rabbit eyes occurred after administration of 10 mg of dry
50% powder, or 0.1 ml of a 10% suspension in mineral oil. No corneal
injury occurred (Du Pont, 1979a).
Mammalian Metabolism
Gardiner (1975) states that substituted uracil herbicides can be
expected to be excreted rapidly by animals (no data was provided for
bromacil) . Two principal urinary excretion products were found to be
5-bromo-3-sec-butyl-6-hydroxymethyl uracil and 5-bromo-3-(2-hydroxy-
-l-methylpropyl)-6-methyl uracil.
Special Studies
Carcinogenicity No signs of carcinogenicity were seen in 2-years
chronic studies with rats and dogs (Sherman and Kaplan, 1975; data
were not included in publication). Charles River-CD rats (36 of each
sex) were fed 0, 50, 250, and 1250 ppm bromacil in a diet supplemented
by 1% corn oil. Dogs (1-2 year old beagles, 3 of each sex) were fed
the same dosages, with levels gradually increasing throughout the
study.
i
Teratogenicity and Reproduction Sherman and Kaplan (1975; data not
included in the report) found no gross manifestations of a teratogenic
effect or abnormalities in bone structure when primagravid rabbits were
fed 0, 50, and 250 ppm bromacil on days 8-16 of gestation, with
offspring delivered on day 29 or 30 by Caesarian section or normal
parturition. No results were reported on fetal weights or number of
resorptions, although these data were apparently obtained.
Newell and Dilley (1978, unpublished data) exposed 50 Sprague-Dawley
rats to vapors /aerosols of bromacil (particle size range of 0.3 to 3.0
um) for 1 to 3 hours on days 7 to 14 of gestation. Concentrations of
bromacil in the air were 0, 38, 78, and 165 mg/m^. At the highest
dose (165 mg/m^) a slightly higher percentage of resorptions was
11-36
found, compared to controls. The study also found dose-related
reductions in fetal weight and caudal ossification (significant at p
<0.01). No effects were noted on weight gain, food consumption,
average number of pregnancies, or litter size. No terata or signs of
gross pathology were noted.
Sherman and Kaplan (1975, data not included in publication) conducted
a rat reproduction study in which Charles River-DC rats (12 of each
sex) were exposed to 0 and 250 ppm bromacil for three generations. In
each generation, no effects were noted on the number of matings,
pregnancies, or offspring in each litter (at birth and at 4, 12, and 21
days). No effects were noted in the body weights of offspring at 21
days. Gross and microscopic examination of third-generation pups
revealed no abnormalities.
Other Chronic Effects Sherman and Kaplan (1975; data not included in
publication) observed a follicular cell adenoma and a slightly higher
incidence of focal light cell hyperplasia and focal folliciilar hyperplasia
in the thyroids of rats receiving 1250 ppm bromacil in a diet
supplemented by 1% corn oil. No abnormalities in hematology,
biochemistry, or urinalysis were noted. Tibia length and organ weights
were not affected at any dosage. In females, at the highest dosage
(1250 ppm) a slight decrease in food consumption and weight gain was
noted (significant at p <0.001).
In a 2-year dog study by the same authors, beagles (1 to 2 years old,
3 of each sex) were exposed to gradually increasing doses of bromacil
in their diet, with in final dosage levels of 0, 50, 250, and 1250 ppm.
No compound-related changes were noted in hematology, biochemistry,
urinalysis, or pathology. At 1250 ppm in both sexes, an initial slight
decline in body weight was followed by a stabilization.
Mutagencity As shown in Table 11-10, most available studies indicate
that bromacil is not a mutagen. Of particular note is the negative
result obtained by Epstein et al. (1972) using a high dose of 1000
11-37
o
I— I
I
<
<
o
Pi
CQ
H
W
H
H
o
1—1
2
o
<
H
P
IS
rt o
'i
CtJ
■M
=
cn
CTJ
(U
CO
^
«^
u
<u
0) o
U
3
vD
u
•M
aor-
C^
3
in
Vi <T>
O^
0
O.
0 1—1
rH
w
01
c
0
•-) ^^
2
1
>^
■»-»
o
•1-1
X
0
I induction (
or loss
o
•iH
4->
C CO
1
t5
•4J
nJ
CO
CO
0
cn
han a
break
•1-1
&0
X
E
-a
week
given
her t
omal
•
"^•^^
60
■M cn
en
a
U)
•
S
o
o
c^ +-
cn
o
«J 0
■♦-»
C
E
E
0
•
E
o
0
•
elated r
f chrom
c
•1-1
i-H
a;
>
o
<4-l
cn
0) cn
•>=? o
cn
U
w
o
fa
0
Q -0
pc3
h 0
3
cn
*
bO
CTl
^—^
•r— )
■*->
2
o
rt
73
u
cn
03
^
C
<n
^
»
'rt
vO
a
o
1— 1
O
s«x
(TJ
qj en
cn «J
!-■
E o^
• f-4 I-H
CO w
(ti
•
u
^-*
■M
nj
cn
•4-»
0
•1-1
1—1
o
CO
o
o^
oci
y
(T)
•
^H
*-4
^J
(tJ
cn
,^4
^
o;
01
0
1—1
u
00
u
a^
6^ -w
00
I
(H
,c
■♦->
(U
»— 1
•t->
c
rt
E
c
E
cn
o
>>
-0
W
0)
■M
cn
cn
3
(i>
0
H
2
CO
Q
1— «
(CJ
0)
C/i
I-H
Ti
•F-t
C
>
u
o
O
• IH
-t->
03
1 0]
c
• r-1
s
^-fi
cn
1
0
S 1;t
0)
t3
en ^
CJ
o
>>
CJ
1— 1
f-H
a;
E
•rH
• f-H
>
o
^
^
•1-*
cn
cn
y
0.
a
rt
•I-*
0
CO
0
o
en
0
CJ
o
CJ
+•>
0
• •H
u
u
^1
03
2
Q
Q
C/^
03
U
>
o
M .1-1
en
to
o
E
o
OJ
o
o
03
CO
cn
u
>
c
o
CJ
C
<u
&0
i)
y
u
D
O
N
(N3
r-
C^
/«-»
^^
o^
^^•"s
ON
>o
>o
^^ r-l
^-v O
1— 1
t*-
c*
fO v-/
ro r~
N^"
o^
o^
00 Tn
00 <T-
fi
i-H
ON . &P
ON rH
•
^^
*-,,-*
^•^
r— ( 1— 1 ra -"-N
1— 1 ^
/--^
1
4->
^, rt ;rr-^
•♦-»
«1
•
o
z y
•
u
I— 1
I-H
(T3
rt
, ♦J 0}
• "— '
(—4
rt
•4->
0}
a
^
^ 0) -a ^
^ nJ
;h
(U
•4->
•h>
•>
V
0)
XJ
"St c "* -^
<!-> a>
i2
c
cn
a
•" o ^ rt
a;
(0
OJ
0
en
C
0
E
e
sD
oirya
nders(
op alar
1976,
>> CT3
C
0
E
E
• p-4
(0
u
•>-i
1— (
0 ^
r— 1
-0
c
c/i
W
C/2
^ <o^
2 c/3 W
<
-^ w
(TJ
rt
0) ^
en «J
E ON
.pH r-l
m N^
Q
W
2
O
i-H
H
• •
Z
W
o
H
u
03
w
o
H
1— 1
1
>^
1— 1
1— 1
H
1— 1
U
t— 1
z
<
o
H
<
H
P
s
en
-♦->
C
E
E
o
O
en
o
•4->
>
en
0
U
• IH
-t-»
Qi
03
>
3
•i-t
I-H
I-H
E
3
a
+->
o
f-H
c ^
3-
•IH
-♦->
0
•l-»
in
a ^
I I
I I
I I
CO
■M
E
,n
a>
3
H-'
en
en
>>
en
C/2
^
■»->
•t-i
en
y
<u
a
H
CQ
fl>
f— 1
1—4
0}
c
>^
o
rt
E
en
1— 1
en
ns
01
C/2
en
o
u
:a
u
Xi
u
CO
0)
■(->
»-H
3.
O
en
en
>* en
en -M
en
< S
Z ^
Q 2
™ rn ^03
p ^ -S 3
t— ' d
I— I s-4 ±;
u o O
0)
03
o
en ii
<
c
o
05
U
fl
•1-1
en
0)
en
a
<u
u
a
mg/kg in a mouse dominant lethal study, considered one of the more
reliable tests of mutagenic potential.
Summary An evaluation of important toxicity data is provided at the
end of this chapter.
3. MOBILITY AND PERSISTENCE
Fate in Soil
A review of registration material led EPA to conclude that "Bromacil is
highly mobile in soil, leaching to depths of 18 to 24 inches" (EPA
1980a). Leistra et al. (1975) found high mobility when bromacil was
applied aainually for 6 to 7 years at rates of 1.6 and 2.4 kg a.i./ha to
a sandy loam and a silty clay loam. (In the sandy loam, the organic
matter percentages were 2.3, 1.9, 1.4, and 0.5% in the 0-20, 20-40,
40-60, and 60-100 cm layers, respectively. In the silty clay loam, the
organic matter percentages were 3.1, 2.5, 1.5, and 0.6.) One year
after final application, residues of 0.01-0.02 ug/g of bromacil were
found down to the 80-100 cm layer in sandy loam and the 50-60 cm
layer in silty clay loam. Highest concentrations (16-33 ug/g) were
found in the 10-20 cm layer in the sandy loam.
Smith et al. (1975) found a similar high mobility in an unspecified soil
in irrigation ditches. Bromacil leached to a depth of 90 cm over a
period of 3 yesirs. When the ditch initially filled with water, the
authors found lower concentrations of bromacil than the other herbicides
tested. They attributed this to the high solubility of bromacil and its
tendency to leach out of the upper zones of soil. Bromacil is soluble to
water at 815 ppm at 25°C (Ouellette and King, 1977).
Reed (1982) found different mobility patterns for bromacil, using three
soils with varying percentages of organic matter. Bromacil was applied
at a rate of 8.96 kg /ha to a sandy loam with 0.56% organic matter, a
silty clay loam with 1.52% organic matter, and a sandy loam with 2.48%
organic matter. Figures II-l and II-2 show the movement of bromacil at
6 weeks and 6 months respectively. In the soil with the lowest per-
centage of organic matter, with limited retention capacity, bromacil
apparently moved through the soil, and was found in very limited
11-40
«
i
(
Concentrations of Bromacil in Soil
Depth in
Soil (cm)
Figure 1
6—8 Weeks after Treatment
4 6
Concentration (ppm)
Figure 2
23 Weeks after Treatment
10
Depth in
Soil (cm)
20
30
4 6
Concentration (ppm)
10
Soil with low organic matter
"~ ^ —Soil with moderate organic matter
^^■^^■"Soil with high organic matter
Adapted from Reed 1982
i
i
{
II-40A
quantities throughout the 30 cm soil profile. None remained after 6
months. In the soil with intermediate amounts of organic matter,
approximately 5 ppm was found throughout most of the profile after 6
weeks, dropping to about 2 ppm after 6 months. In the soil with the
highest organic matter content, 10 ppm bromacil was retained in the
upper layers after 6 weeks. After 6 months, concentrations increased
in the lower depths while remaining high in the upper layers.
Helling (1970) also found the mobility of bromacil to depend on organic
matter. According to Helling and Turner's mobility classification sys-
tem, bromacil is in class 3 to 5 (with 5 representing the greatest
mobility) when tested in soils with high to low organic matter content.
Bromacil can be considered persistent in soil. In a review of its reg-
istration material, EPA found the hcilf-life in soil to be 7 months
(unspecified soil) (EPA 1980a). In a sandy loam used by Leistra et al.
(1975), discussed above, the rate of decrease in concentration corre-
sponded to a hcilf-life of 8 months. A somewhat shorter persistence was
found by Gardiner et al. (1969), who determined the half-life in a silt
loam to be 5 to 6 months, and by Jolliffe et al. (1967), who found
half-lives of 3 to 6 months in unspecified California soils. When radi-
oactive-labeled bromacil was applied to unspecified soil in the field,
68.8% remained after 5 weeks, 63% after 14 weeks, and 23.5% after 1
year (EPA, 1980a).
Microbial activity is the primary mechanism of breakdown of bromacil in
the soil (Torgeson and Mee, 1967). The major metabolic product is
5-bromo-6-hydroxymethyl-3-sec-butyluracil (EPA, 1980a).
Photodecomposition and volatilization are not expected to be significant
routes of loss. Losses of bromacil from soil were found to be less than
0.1% per week (Hill, 1971).
Persistence in Water
Only limited information is available on the fate of bromacil in water.
Bromacil is not easily photolyzed, but does form 5-bromo-6-methyluracil
11-41
at a very low rate. Degradation by hydrolysis does not appear to be
significant (EPA, 1980a).
Indicators of Potential Ground Water Contamination
Table 11-11 provides information on parameters associated with the
mobility of bromacil. These parameters, and their associated thresh-
olds, have been suggested by EPA for use in assessing the potential
for pesticide contamination of ground water. A discussion of these
parameters and thresholds, and the methods for arriving at designated
values for individual herbicides, is presented in the main body of the
report as part of the discussion of the fate of herbicides in the envi-
ronment .
4. TOXICITY TO NON-TARGET ORGANISMS
Birds and Fish
Thomson (1975) and a study by EPA (1975a) state that bromacil is
non-toxic to birds and fish. The 8-day dietary LC-^ was found to be
>10,000 ppm for both mallard ducklings and bobwhite quail (Du Pont,
1979a) . The 48-hr LC(.^ values for bluegills and carp are 71 ppm and
164 ppm, respectively. The 96-hr LCj.. for fathead minnows is 182
ppm. Rainbow trout show greater sensitivity, with a 72-hr LC-^ of 28
ppm (Du Pont, 1979a).
Lower Aquatic Organisms
Limited information suggests that bromacil is non-toxic to lower aquatic
organisms. The 3-hr TL values for crayfish eind water fleas are both
m
>40 ppm. The 72 -hr TL for crayfish is 230 ppm.
Bees
Atkins et al. (1976) classifies bromacil as "relatively non-toxic" to
honey bees.
11-42
TABLE 11-11
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
BROMACIL
Indicator
Solubility
K
DC
Speciation at pH 5
Hydrolysis half -life
Photolysis heilf-life
Vapor pressure
Value for Bromacil
815 ppm at ZS^C
72
ND* (probably
neutral due to 2
weakly basic and no
acidic groups)
Appears to be
stable (EPA, 1980a)
Appears to be
stable (EPA, 1980a)
2.5 X 10
at 25°C
-7
mm Hg
Threshold
>30 ppm
<300-500
Anionic
(negatively charged)
>6 months
>3 days
-2
<10 mm Hg
* ND = no data.
Toxicity Data Evaluation
Insufficient information is publicly available on the carcinogenicity and
teratogenicity of bromacil. One carcinogenicity study has been accepted
by EPA. It is reasonable to assume that this test did not show positive
results, since no rebuttable presumption against registration was trig-
gered. Another carcinogenicity test is required by the registration
standard. Other data requirements yet to be filled by the manufacturer
include a chronic feeding study, and one reproductive effects study.
(Other deficiencies include data on acute toxicity to estuarine and
marine organisms, avian single-dose toxicity, acute fish toxicity, acute
toxicity to aquatic invertabrates , hydrolysis, photodegradation in water,
metabolism in soil and aquatic organisms, leaching potential, dissipation,
and accumulation in crops, fish, and lower aquatic organisms.) No
further mutagenicity tests are required. Again, it can be assumed that
the mutagenicity tests on file do not show bromacil to be a mutagen,
since no further regiilatory action has been taken. The majority of
11-43
tests shown in Table 11-10, including a mouse dominant lethal study,
strongly suggest that bromacil is not a mutagen.
Regarding teratogenicity, the data cited above are consistent in the
indication of no teratogenic effect. One additional test, however, is
needed to satisfy EPA requirements. One teratogenicity test heis
edready been accepted by EPA.
No data in EPA registration files concerning bromacil were generated by
IBT.
11-43. 1
E. 2,4-D
1. INTRODUCTION
2,4-D is the common name for the herbicide 2,4-dichlorophenoxy acetic
acid, available from Dow Chemical U.S.A. and others. It is produced
® ®
in numerous formulations, some of which are Weedone , LV-4 , Esteron
99 Concentrate, Weedar 64 , DMA-4, Verton 2-D , Agrotect ,
<8> (8) ® ® ® ,
Barwell , Phenox , Weed-B-Gon , Miracle , and Formula 40 . (TRW,
1981; EPA 1980b). These formulations involve a variety of forms of
2,4-D, including sodium salts, amines, high volatile esters, low volatile
esters, and oil-soluble mixtures (Thomson, 1975). The structure of the
acid is:
0
II
0-CH -C-OH
More than other herbicides, the physical and chemical properties of
2,4-D are dependent on the form of the active ingredient. Table 11-12
shows some of the variation in solubility for various forms of 2,4-D.
Other physical and chemical properties are presented below in the
discussion of the fate of 2,4-D in soil and water.
2. TOXICITY
Acute Toxicity
In a report by NRCC (1978), 2,4-D was considered moderately toxic,
based on the oral LD-. values summarized in Table 11-13. The oral
LD_- values for the acid form range from 100 mg/kg in the dog to 541
mg/kg in chicks. Both Drill and Hiratzka (1953) and Rowe and Hymas
(1954) noted that the salts and esters were less toxic than the acid
form.
11-44
TABLE 11-12
VARIATIONS IN THE SOLUBILITY OF 2,4-D
Form
Solubility in Water
Acid
Diethylamine salt
Butoxyethanol ester
N-oleyl-1,3 propylene-diamine salt
®
DMA-4 (dimethylamine salt)*
®
Esteron-99 Concentrate*
®
Formula 40
0.09g/100g @ 25°C
300g/100g @ 20°C
Insoluble
Insoluble
Infinite
Emulsifiable
Infinite
As cited by Dow Chemical U.S.A. (1978, 1980); all others as cited by
TRW (1981).
The Material Safety Data Sheet for Weedar 64® (the DMA salt of 2,4-D
acid) by Union Carbide (1977) cited the oral LD_- value for male albino
rats as 1615 ± 170 mg/kg for the salt formulation. This sheet reported
the dermal LD_ value as greater than 500 mg/kg, and the inhalation
LD-- as greater than 288.6 mg/1, both for the rat.
®
The Material Safety Data Sheet for Weedar 64 stated that it was an eye
irritant to male rabbits. The label for DMA-4 by Dow Chemical U.S.A.
states, "Warning. Injurious to eyes, may cause skin irritation." The
Material Safety Data Sheet for the same substance reported that "eye
contact may cause moderate irritation and also moderate corneal burn.
Skin contact may cause moderate irritation and possibly a superficial
burn." Approximately the same conclusions were drawn on the
® ® /
Material Safety Data Sheets for both Esteron 99 and Formula 40 (Dow
Chemical U.S.A., 198 Oab).
11-45
(U
u
u
o
en
'■"^
rt<
*— *
^-^
m
^->
cr*
^
tt
in
■«^
rH
''"^
Ifl
in
rH
in
:—{
a
f— (
1—1
(0
S
1-1
1— 1
E
cn
S
•
1— 1
>N
>^
Jh
>^
0
X
c
K
X
2
a;
'0
l-H
T3
c
T3
TD
>
c
^
c
c
C
0
rt =
CiO =
OS
rt
(ti
c
3
C
0
<u
ai
H)
,_,
(U
^
J
^
r— 1
^
0
^
0
o
0
u
O
0
pc5
2
oii
Q
e^
CQ
J
to
a;
T3
(U
1
bo
>*
,^
in
«k
sO
fVJ
bO
t*-
C=t4
o
E
oo
in
o
o
o^
o
r— I
V
o
o
o
O
vO
D-
o
(^0
vD
o
■^
o
00
CO
in
o
o
o
CO
ro
CO
in
ro
•^
r— t
in
CT-
ro
ro
o^
rH
1
o
V
V
r— (
rH
1
1— 1
>^
in
A
1— 1
Q
Cd
u
J
l-H
CQ
X
<
o
H
H
X
Cn
(X4
b
b
b
U
(U
:s
2
1
1
m
*
«»
««
b
1
1
•^
<
C/3
2
2
2
2
2
w
0)
<u
y
(0
<u
s
&
0
C/2
2
o
■ rH
-t->
03
O
nj nJ
<
&£
bO
fH
• l-H
a
Q-
CO
CJ
03
cn
w
(U
cn
<u
OJ
rili
X
^
<t>
r^
c
C
u
o
o
tn
O
fh
• rH
&0
• rH
•l-<
• rH
■♦->
3
•r*
3
3
o
rC
rfl
rd
03
o
-C
J
o
Q
o
o
(U
a
1
c
<
U
•4->
w
0
•r4
<
pci
S
u
(»
r— I
>^
Xi
o
•*J
3
CQ
rr
in
o^
1— 1
>>^
(0
<i
S
>>
X
13
fi
<i)
rt
o
u
(U
3
^
o
o
en
pti
>*
in
a-
r-{
— '
/-«>
Ul
CM
nJ
r-
a^
E
r-i
>>
Nil*'
X
>
0
^ = =
••-1
c
c
;3
0)
03
Pi
%o
l-H
CT^
^_^
■^^
^_^
/— N
^.^
*^^
i—l
0)
(3
f— 1
CO
1— (
in
1— 1
I—l
•
)4
r— *
0)
El)
(U
^"^
tn
(U
en
(U
rt
rt
>
-0
In
• 1-4
•
r— 1
E
In
E
In
1—1
u
CTJ
rt
•«-»
l-H
X
T3
rt
•»4
-0
O
(U
^3
o
T3
U
;s
^3
>
o
C
o
-a
c
C
T3 _
= S
^
rt
(L>
03
(U
OJ
0
1— t
1—1
»l-4
O
1—1
^
S
•1— »
• f-4
0
• rH
o
• rH
CQ
J
Pi
X
pci
E
9^
M-l
u
^^
Q
^-v
•<->
(U
P
1
C
• r-l
O
o
in
1— <
en
■4->
2
I—l
Px^
^
CO
I—l
o
CO
'O
o
o
2
O
o
r^
vD
oo
rr
c
•1-^
o
c^
in
O
U
>^
in
1—1
o
vO
H
I—l
Q
1
o
o
1
o
00
U
fV3
1
O
CO
CO
o
I—l
CO
1
l-H
l-H
O
H
W
W
J
H
CQ
<
U
U*
[S4
Cl4
u*
1
1
2
<
en
2
o
tn
in
o in o in vo I— I
o c^ vo o vO in
r— I CO CO 00 nO in
I I
o o •^ o
o o 1— H CO
O 00 (M f-
1-4 A
I I
&0
bO
!30
bO
•IH
•PH
.1-1
•FH
a
04
a
cu
cn
0)
rt
4->
OJ
Oj
«J
4->
>H
(U
0)
• rH
o
0)
V
(U
D
<u
<u
•iH
9)
u
en
c
S^
en
en
c
en
en
c
c
J2
^
(U
3
■*-»
■l-H
XI
•M
3
4->
3
»f-i
•«-»
3
3
■M
-M
• rH
• rH
^
C
•fj
a
0
rt
3
rtJ
05
0
OJ
0
3
01
o
0
OJ
OJ
3
3
<fl
0
A
n
2
Pi
O
Pi
p:;
2
Pi
2
O
Pi
2
:s
Pi
p::
a
O
Pi
2
ei
(fl
c
^
0
<u
• rH
•4->
■*■*
en
OJ
<u
^^
3
l-H
£
>
u
0
•M
3
ta
CQ
en
a
o
!h
a
o
en
u
o
-»->
P^H
OJ
-M
en
l-H
•«->
OJ
E
en
13
en
3
• rH
E
S
en
3
en
• IH
3
OJ
TS
• IH
■*->
o
13
o
en
O
0^
cn
4
(U
o
u
o
IT)
01
E
X
c
o
Pi
u
lU
•«-»
y"v
nJ
c^
2
c^
a>>
<
i—i
w
•^
•
(U
P
0)
f^
C/3
rt
u
n)
a
Q
U
>N
■*->
^
0
OJ
Q
m
0)
■«-»
. o^
<ci
en +*
& a
<U Q
> (U
O nj
H
O
o
CO
I— I
I
I
fa
o
>^
H
I— I
U
X
o
H
W
H
D
U
<
S
o
in
Q
o
tn
fa
o
O
o
o
<M
1— 1
fO
c^
OO
C^
(N3
o
I fa :s
o
1
o
o
o
o
00
I
a
T
c
%
t
fa
en
•rH
o
•i-i
a
nt
0)
C
•i-t
O
^
.£} '4-> ■«->
■<->
fO rt rt
nJ
Pi Cri Oi
oi
j3
■M
c
en
E
*^
0
(U
.!-<
It
• f-^
■4-»
TD
U}
•*-»
(n
t— 1
(U
o\o
<u
3
£
o
03
1
<
CO
•
•1-4
E
O
2
•>— «'
rt
fa
cu
Q
"^ <u
@ c
^ *S
^ c
CTJ
c nj
^^
fa
00
u
c
o
I >, tn
W
Sub chronic Toxicity
Drill and Hiratzka (1953) reported that dogs could tolerate 10
mg/kg/day of 2,4-D, 5 times per day, for 13 weeks without any
significant adverse effects. The dogs could not tolerate 20 mg/kg for
the same time period (adverse effects not stated in the 1978 NRCC
review). Row and Hymas (1954) gave oral doses of 3, 10, 30, 100, and
300 mg/kg of 2,4-D to rats, 5 times per week for 4 weeks. No
observable effects were noted at concentrations below 30 mg/kg, but at
30 and above, a depressed growth rate, liver pathology, and
gastrointestincd irritation were noted. Rats given 300 mg/kg died
within the 4-week period.
Mammalian Metabolism and Elimination
14
Khanna and Fang (1966) fed 1 to 100 mg of C-labeled 2,4-D to rats
and monitored expiratory gases, urine, feces, and various tissues.
From 75.5% to 93.3% of the 2,4-D (mainly as parent compound) was
excreted within 144 hours (most within the first 24 hours). At least
one unidentified metabolite was also found in the urine. Similar results
have been reported by Clark et al. (1964) on sheep, and by Lisk et al.
(1963) on steer.
Khanna and Fang (1966) noted that the time necessary to eliminate
2,4-D from the body was dose-dependent. Rats eliminated 1 to 20 mg
within 24 hours, but 100 mg required 144 hours for a 75% recovery.
However, Fang et al. (1973) showed that assimilation efficiency does not
appear to be affected by the size of the dose.
Erne (1966) noted that the amine and alkali salts of 2,4-D were readily
absorbed in the gastric region, but that the ester was incompletely
absorbed. The EPA (1977) noted that all cholorophenoxy acids, salts,
and esters were absorbed across the gut wall, the lung, and skin, but
were not stored in significant amounts in fat. Excretion usually
occurred within hours, or at most days, usually in the urine. Erne
(1966a, b) stated that the plasma half-life of 50-100 mg/kg of orally
introduced 2,4-D was 3 to 12 hours in rats, pigs, and calves. Pigs
eliminated the 2,4-D mainly in the urine, primarily as the parent
11-49
compound, but also as unidentified acid-hydrolyzable conjugates.
Penetration into the central nervous system and adipose tissue was
restricted, but placental transfer was rapid in pigs.
Fang et al. (1973) reported that small amounts of phenoxy herbicides
were passed to the young through their mother's milk. The diet-to-
milk concentration factor, however, was less than 10 to 3 (Bjerke et
al., 1972).
Elo and Ylitale (1977) introduced a subcutaneous dose of 250 mg/kg into
rats. Within 4.5 hrs, 67% of it was located in the plasma. A
breakdown product, 2,4-dichlorophenol, was identified. H. E.
Christensen et al. (1974) gave an oral LDr« value of 580 to 1625 mg/kg
for mice and rats for this substance.
Graff et al. (1972) injected 250 mg of 2,4-D intraperitoneally and
reported that there was a reduction in the synthesis of acid-soluble
organic phosphate in muscles. The authors concluded that the
pathogenic mechanism of 2,4-D was the uncoupling of oxidative
phosphorylation .
Special Studies
Carcinogenicity There has been considerable controversy regarding the
potential for 2,4-D to cause cancer. Most of the controversy has
involved a study by Hansen et al. (1971) who administered 0, 5, 25,
125, 625, and 1250 ppm 2,4-D to male and female Osborne-Mendel rats
for 2 years. He noted no adverse toxicological effects or increased
incidence of tumors above control values. As part of the same
investigation, no increased incidence of tumors was noted in a 2 -year
dog study in which beagle dogs were given 0, 10, 50, 100, or 500 ppm
2,4-D in their diets.
There is general agreement that the dog study does not show 2,4-D to
be a carcinogen. Melvin Reuber, a toxicologist at the National Cancer
Institute, qualifies his support of the study by noting that 2 years is
an insufficient duration for a dog study. Dr. Reuber' s primary
11-50
disagreement, however, is in regard to the rat study. Reuber (1979)
believes that the histological examination of rat tissues was inadequate
in that only grossly visible neoplasms were sectioned, and therefore
microscopic neoplasms may have been missed. He also faults the
practice of performing detailed histopathology on six rats of each sex in
the high dose group and controls, with reduced tissue consideration at
other treatment levels. Reuber claims, furthermore, that he reviewed
the complete set of raw data and histologic sections. His conclusion is
that 2,4-D is carcinogenic in rats.
Reuber' s statements regarding inadequacies in the study's methods are
justified. However, it must be noted that the experiment was
conducted in 1964 and reported in 1971; the state of the art regarding
these tests has changed considerably since that time. Regarding his
conclusion about the carcinogenic potential of 2,4-D, it is difficult to
critique his judgment in the absence of the raw data. Some of his
statements, however, are questionable. For example, he notes a
dose-related increased incidence of malignant neoplasms for all sites in
male rats. His data, however, indicated little change in incidence: 36%
(9/25) for the 25 and 125 ppm groups, 25% (6/24) for the 625 ppm
group, and 39% (9/23) for the 1250 ppm group.
The Hansen data for rats were reviewed by the National Cancer
Institute, the EPA, and the editorial staff of the Journal of Toxicology
and Applied Pharmacology, all of whom agreed with the author's con-
clusions (although probably without a reexamination of the histologic
sections). The greatest value in Reuber's criticism may be in pointing
out inadequacies in study technique and the need for further study.
Therefore, this report concludes that no conclusions regarding the
carcinogenic potential in rats can be made on the basis of this study,
i.e. it presents no clear evidence for or against the carcinogenic
potential of 2,4-D.
In another study, Innes et al. (1969) found no increase in the
incidence of tumors above control values in male and female mice
(C57BL/6 X C3H/Anf) or C57BL/6 x AKR) mice given an oral dose of
11-51
I
i
46.4 mg/kg by gavage on days 7-28 of age, followed by an addition of
2,4-D in the diet for approximately 18 months. Dietary additions were
111 ppm for the isopropyl ester, 149 ppm for the butyl ester, and 130
ppm for the isooctyl ester.
Vettorazzi (1975), as reported in a review by Arthur D. Little, Inc.
(1979), found no increased incidence of tumor formation in mice fed
2,4-D orally for their lifespan.
Eriksson et al. (1981), in a case-control study, found indications that
occupational exposure to phenoxy acids (2,4,5-T, 2,4-D, MCPA,
mecroprop, and dichlorprop) and chlorophenols might constitute
roughly a six-fold increase in risk for the development of soft tissue
sarcomas. As is often true for such studies, the investigation involved
a relatively small sample size. It is difficult to draw conclusions
regarding the effect of 2,4-D, separated from the effects of other
chemicals to which exposure occurred.
One study showed the proliferation of peroxisomes following
administration of 2,4-D. Vainio et al. (1982) showed an increase in the
mean frequency of peroxisomes from 17.7/100 \xm^ (controls) to 27.3/100
um^ in liver cells of Chinese hamsters given nine daily doses of 100
mg/kg of 2,4-D by gavage. Vainio and his co-workers suggest that
2,4-D may fit into a novel class of compounds that are carcinogens in
rodents and whose mechanism of action appears to involve the excessive
production of hydrogen peroxide-generating enzymes. Liver cells may
thus be exposed to the cytotoxic or DNA-damaging potential of
hydrogen peroxide, leading to the subsequent development of liver
neoplasia. This peroxisome proliferation response, however, does not
occur in humans, monkeys, rabbits, or guinea pigs (Cohen and Grasso,
1981). These results are therefore of questionable relevance to an
assessment of risk to humans.
A slight reversible effect was noted in bovine fetal muscle cells exposed
in culture to 2 or 20 mg/1 of 2,4-D in a study by Basrur et al. (1976).
Cultures exhibited an initial drop in total cell counts at 48 hours, but
11-52
recovered in 96 hours. The percentage of mitotic cells in cultures
treated with the higher dose of 2,4-D was also decreased at 24 hours,
but was within normal values at 48 hours.
Teratogenicity / Reproduction There is considerable disagreement over
the interpretation of tests that assess the teratogenic /reproductive
effects of 2,4-D. Conclusions regarding the results of these tests are
generally either that 2,4-D is a "weak teratogen" or that it does not
cause "true teratogenic" effects. The review conducted for this report
concluded that
1. At very high doses (1000 mg/kg and above), there seem to be
teratogenic and/or reproductive effects;
2. At doses below 50 mg/kg, there seems to be little or no
teratogenic or reproductive effect;
3. At doses of 50-150 mg/kg, adverse effects occur in some
studies and not in others.
There is considerable disagreement among previous reviewers regarding
the significance of the effects that occur at 50-150 mg/kg, and also
whether they should be considered teratogenic, embryotoxic or
fetotoxic. Disregarding the semantic difficulties, the position of this
report is that the observed malformations should be considered
significant, whether or not they affect the organism's chances of
survival. However, the lack of a clear dose response in some studies,
the low incidence of abnormalities in most studies, and the absence of
any adverse effects in other studies, indicate that 2,4-D can only be
considered, at most, a weak teratogen. Furthermore, it should be
noted that equivalent doses of 50-150 mg/kg in humans (3.5 to 10.5 g)
are highly unlikely even for a worst-case exposure.
The following is a brief discussion of some of the key studies that
examine the effects of 2,4-D when administered at doses of 50-150
mg/kg. For further detail (and alternative views) the reader is urged
to read two reviews, one by Mullison (1981) and one by the
Epidemiological Studies Laboratory of the State of California (1980).
11-53
In a study by Collins and Williams (1971), 20 to 100 mg/kg 2,4-D was
administered to hamsters on days 6 to 10 of gestation. Occasional
abnormalities (usually fused ribs) were noted, along with decreased
fetal viability. Neither of these effects was dose related. The number
of fetal abnormalities was not statistically significant.
Khera and McKinley (1972) noted a slight increase in fetopathology and
incidence of fetal skeletal anomalies in pregnant Wistar rats at levels of
100 or 150 mg/kg /day. Effects included delayed ossification and wavy
and lumbar ribs. The 2,4-D was administered in the form of isooctyl
and butyl esters and the butoxyethanol and dimethylamine salts. No
adverse effects were noted at 25 and 50 mg/kg /day. Similar skeletal
abnormalities were observed by Schwetz et al. "(1971) at doses of 50
mg/kg and above. The effects were dose-related. No significant
adverse effects were noted at doses of 12.5 and 25 mg/kg.
No evidence of embryo or fetal lethality or maternal toxicity was seen in
groups of CD rats given daily oral doses of either the propylene glycol
butyl ether or isooctyl esters of 2,4-D at molar equivalents of 0, 6.25,
12.5, 25, or 87.5 mg 2,4-D/kg/day on days 6 through 15 of gestation.
No gross or soft tissue anomalies were observed. An increased number
of fetuses in the two 87.5 mg groups had fourteenth rib buds, but this
observation was considered to be within the normal range of variation.
Postnatal growth and survival of pups in the 87.5 mg groups were not
adversely affected (Unger et al. , 1981).
Courtney (1977) noted an increase in the percentage of cleft palates
when 0.56 and 1.0 mM/kg (approximately 124 and 221 mg/kg) 2,4-D was
administered to CD-I mice. Cleft palate occurred in 5%-16% of the mice
(compared to 0% in the control group) for two esters and the acid.
Cleft palate was observed when oil or DSMO was used as a carrier, but
not when sucrose was used as a carrier.
Konstantinova et al. (1976) noted no adverse effects on embryos of
random-bred female rats given either 2,4-D (0.1, 1, or 50 mg/kg) by
gavage during gestation. The 2,4-D was given daily through day 20 of
11-54
gestation. Because of discrepancies between the text and tables, the
exact results are difficult to determine. However, it appears that 50
mg/kg induced an increased incidence of fetal hemorrhages and that no
effect was seen at lower doses.
In a three-generation rat reproduction study (Hansen et al. , 1971),
Osborne-Mendel rats were given 100, 500, and 1500 ppm of 2,4-D. At
the highest dose, the body weights of weanlings were markedly
reduced, as was the percentage of pups that survived to weaning.
These effects were not observed at 100 and 500 ppm. No effects on
fertility or litter size were observed at any dose. No terata were
reported; however, there was no specific examination for teratogenic
effects.
Carmelli et al. (1981) found no positive association between occupational
phenoxy herbicide exposure in males and subsequent spontaneous
abortions in their wives. A suggestive association with overall 2,4-D
exposure was noted in an isolated subgroup of wives of young
forest /commercial workers, but not for the same age group of farmer's
wives, indicating that the suggestive association may be attributable to
chance alone.
Mutagenicity Although there is conflicting data, the most reliable tests
indicate that 2,4-D is not a mutagen. As indicated in Table 11-14, no
mutagenic response was found in experimental data that measure
heritable genetic lesions in whole animal bioassays. Both positive and
negative findings are observed in the remaining battery of cellular/ in
vitro studies. Positive findings in one or more of these tests, though
they may suggest the possibility of heritable genetic lesions, are insuf-
ficient to outweigh the findings of the whole animal bioassays.
11-55
(0
u
u
o
^3
■M
c
CO
a
w
00
C
o
o
CO
C
l-H
• 1-1
a.
CO
I— I
T3
C
(U
■M
O
>-
r-
r-
t^
CT'
o^
^^
r-{
l-H
c*-
s,^
r-
^-v
o«»
•
•
■^
fH
l-H
1— t
c^
v^
OJ
(d
o^
l-H
•'"^
^
•M
•«-»
>—'
^
c^
r-H
<U
(U
«J
o
ao
60
>>
rt
i-H
CO
C
•i^N
&0
•1-1
t3
E
J3 =
0)
■4-»
■M
•s
cu
ta
<
M
NI
CO
C!
O
Q
I
CM
CO
r— 1
H
1
C/)
1—4
P:^
1— 1
H
w
J
>-•
CQ
H
<
1— (
U
t— 1
z
o
<
H
D
CO
•M
c
E
E
o
O
3
CO
0)
130
^
c
bo
0
S
•f-l
o
u^
a>
c^
•S bO
co
CO
0
CU iiO
73
.^- E
l-H
(U in
fd
•— I (N]
Vi
bOrH
0
C
un W o
O
S
o
o
m
I
o
o
I-H
V
-o
E
o
CO
o
E
o
u
u
00
o
&0
c
CO (U
— ™
bO E
3. O
o X
E
o
CO
o
E
o
X!
CJ
S "I
■^ o -t->
dO in rt
I Jh
r-H <U
• J2
O 03
rj
o
o
bO
E
in
? ^
. '
O l-H
nj
^
•M
lU
1— t
•t->
C
rtJ
E
a;
•11
E
CO
o
>>
'V
C/2
(U
■M
CO
CO
3
d)
0
H
2
0
>
• fl
>
'O
c
(U
^
^
CO
C
o
<u
T13
!h
■4^J
^5
E
o
Xi
(U
a
rtj
0)
c
E
1—^
>
• 1-4
CO
0
-"2
a
0
CO
o
CO
(U
o
CO
1-1 .1-1
u
o
;3 c
Q
2
a: -^
CO
l-H
r-H
(U
u
o^
c^
>
u
(U
-M
CO
E
CO
<u
C
•i-«
rt ^-.
-a g
^ E
0) --
E (U
CO O
CO
o
E
o
(T3
u
o
03
CO
o
CO
•^
0)
CJ
Q
>>
<u
E
(TJ
0
•PH
u
03
CO
• IH
>
o
!h
CJ
0)
nJ
CJ
in
c
o
••1
c
E
o
u
0)
n£>
,,^
vO
„-v
OO
C^
m
r-
r— 1
o^
CT-
oo
a^
OO
i-H
1— 1
o^
r— 1
o^
^■^
^ —
I— (
"^ '
r— H
•
/«-s
•
1— 1
•
•
13
•^
rt
,_,
%
c-
(tJ
13
■4J
a^
■M
■*-*
V
i—t
(U
•«->
0)
•M
's^'
(U
<u
05
3
(0
0)
bO
3
rt
:3
en
■♦->
u
u
3
•1-1
>>
•j-i
•i-t
CO
o
rt
s:
0
^
^H
Ui
fa
in
2
W
PL.
i^
r-
^^
..—s
c-
(NJ
(M
/^^
^—^
cr-
r-
C-
r-
vO
/"-N
r— 1
o^
CT-
^>.
r-
c^
fO
-^
r— (
1— (
r— 1
a^
a-
OO
N^
>.^
00
1— 1
1—1
o^
•
a-
*— '
0)
(0
nJ
• I-H
u
o
2
rt ^* <u
0)
a;
^s]
CT3
<U
c
c
0
0
en
en
u
Vi
a;
(U
-0
73
c
C
<
<
-t->
en
o
u
PLI
^
E
o
Q
1
^~»
"^r
Q
«
W
OJ
P
Z
• •
en
1— t
C/5
•*->
H
2
S
E
0
0
U
0
H
1— (
1
H
1— I
0
1
l-H
0
I-H
I— I
<
Z
w
0
<
H
2
1— 1
en
0)
>
(U
en
(U
(Nl O, )h
o c X
CM .5 <u
o
o
01
3.
in
(30
a.
o
lT)
(0
<u
o
E
o
o
o
^
en
.1-1
(0
P-H
0)
■ I-H
s
u
en
^
(U
>>
S
C
3
■*->
0)
en
en
0
0
>>
u
en
en
02
OJ
«
^
X
0
•«->
0
;-i
• fH
en
0
<A
0
<u
rt
s
rt
H
03
CQ
en
en
O
o
o
nl
o
u
0)
o
en
bO
C
C
•1-1
I
(— I
o
<
2
Q
W
1—1
§
E
l-H
ffl
w
E
H
^_ «
o ao
03
en j2
C n
OS
•(->
£
01
u
CO
•rH
CO
0)
rC
•4->
c
>>
(0
< „
Zen
Q ^
>>
(U o
3 01
TO 0-
^%
1—1
01
C
o
s
■1-1
C
o
oa
u
01
a.
{
Dioxin Contamination of 2,4-D
Cochrane et al. (1980) analyzed 58 samples of 2,4-D representing 1980
supplies available in Canada. Ester and amine formulations were found
to contain dioxins in the form of 2,7-dichlorodioxin, 1,3,7-tri-
chloro-dioxin , and l,3,6,8-/l,3,7,9-tetrachlorodioxin. About 30% of the
amine formulations were found to contain one or more of these dioxins
in concentrations ranging from 5 to 587 ppb total dioxin. About 95% of
the esters contained one or more dioxins in concentrations ranging from
35 to 23,815 ppb. Acid formulations did not contain any dioxin. The
level of detection in this study was 1 ppb .
Internal EPA correspondence (R. Harless, Health Effects Research
Laboratory,- 1981) reports results on laboratory analysis of 2,4-D for
dioxin contamination. In this investigation, three samples previously
found to contain some dioxin were analyzed and were found to contain
2,7-dichlorodioxin (2,7-DCDD) at concentrations of 73.5 to 184 ppb,
along with other dichlorodioxin isomers at lower concentrations. Two
out of the three samples were found to contain 1,3,6,8-tetrachlorodioxin
at concentrations of 3 and 5.5 ppb. Other tetrachlorodioxin isomers
were found at lower concentrations, but no 2,3,7,8-isomer was detected
(detection limit not given). Trichlorodioxins were not analyzed, due to
lack of an adequate standard.
The dioxin isomer that has been the subject of considerable attention
because of its high toxicity is 2, 3, 7, 8 -tetrachlorodioxin. As stated
above, this has not been found in 2,4-D. Limited information is
available on other dioxins. One 2-year mouse study (NCI, 1979) found
some suggestive evidence of carcinogenic potential of 2,7-dichlorodioxin
in male mice fed 5000 and 10,000 ppm in their diet. A dose-related
incidence (p = 0.008) of hepatocellular adenomas or carcinomas were
found in male mice, although the report notes a historical incidence of
this lesion in the strain of mice used in the experiment (B6C3F1). In
male mice, significant increases were found at low doses, but not at
high doses, in the incidence of combinations of leukemia and lymphomas
and combinations of hemangiosarcomas and hemangiomas. No evidence of
tumor induction was noted in female mice.
11-58
As part of the same study, Osbome-Mendel rats (35 of each sex) were
fed 5000 and 10,000 ppm 2,7-DCDD over a 2-year period. No induction
of tumors was noted in males or females.
Khera and Ruddick (1973) of the Canadian Department of National
Health and Welfeire, performed a teratology test on 2 , 7-dichlorodioxin .
Pregnant Wistar rats were treated orally on days 6 through 15 of gesta-
tion with 250-2000 yg/kg/day of 2,7-TCDD in an anisole-com oil car-
rier. At higher doses (100-2000 ug/kg) the occurrence of myocardial
lesions was noted. (At 1000 and 2000 ug/kg, the number of fetuses
with lesions of the myocardium was 2 and 7, respectively. No such
lesions occurred at lower doses or in the control group.) No effect was
observed at any dose in litter size, resorptions, fetal weight, or skel-
etal formation, nor in pup weight, growth or survival. It should be
noted that the authors did not mention the incidence of myocardial
lesions in their abstract but stated, rather, that the substance "pro-
duced no significant effects." It is possible that the myocardial lesions
may be a toxic response, since growth of cardiac tissue was suppressed
and the lesions occurred at very high doses for dioxins. Dioxin is
introduced into the environment at concentrations that are several
orders of magnitude lower than the herbicide active ingredient. The
lack of response at 500 ug/kg may therefore represent an adequate
margin of safety for teratogenesis.
Summary An evaluation of important toxicity data is provided at the
end of this chapter.
3. MOBILITY AND PERSISTENCE
Fate in Soil
A considerable amount of study has been given to the fate of 2,4-D in
soil. This section is divided into separate discussions of leaching/
adsorption, runoff, persistence /degradation, and volatilization.
Leaching / Adsorption Data on the mobility of 2,4-D in soil is somewhat
conflicting. The overall variability in results may be due to differences
11-59
in soil characteristics, since the percentage of organic matter strongly
influences 2,4-D mobility, as does clay content to a lesser extent.
Also, some studies show that 2,4-D mobility varies with the form of the
herbicide, i.e., whether it is in the form of an acid, a salt, or an
ester.
The available field studies regarding the leaching of 2,4-D show both
high and low mobility. High mobility was shown by a study in which
both the 2,4-D amine and the ester were applied to silty loam soil
(application rates not given) , followed 1 day later by "simulated rain-
fall." After 2 days, 2,4-D had leached to a depth of 24 cm; after 5
days, it had moved to a depth of 40 cm. Thirty days after application
it continued to move downward in the soil (depth not given) (Wilson
and Cheng, 1976).
Low mobility was shown by Burcar et al. (1966), who found that the
isooctyl ester of 2,4-D (after being hydrolyzed to the acid in the soil)
remained for the most part in the upper 5 cm of soil, with no lateral
migration observed. Similar results were found by Smith (1975), who
found only negligible amounts of 2,4-D below 5 cm at the end of one
growing season.
Moderate mobility is indicated by the results of a study by Bornett
et al. (1967) who found that 2,4-D esters moved to a depth of 15 cm
(only trace amounts were found below this level) , although most of the
2,4-D remained in the top 8 cm. Penetration into the 8 to 15 cm layer
was greater for the amine salts than for the esters.
In a study by the United States Air Force Academy (Young et al.,
1974) extremely high amounts of 2,4-D cind 2,4,5-T butyl ester mixtures
were applied to Utah soils at a depth of 10 to 15 cm. After 282 days,
residues were found throughout the 91 cm core sample. However, 90%
of the residues had moved only 15 to 20 cm downward (i.e., they were
found in the top 30 cm of the soil profile) .
Laboratory studies indicate a greater mobility for 2,4-D than do field
studies. The National Research Council of Canada (NRCC) stated in its
11-60
review of 2,4-D that recent studies (Eshel and Warren, 1967; Helling,
1971a, b, c; Helling and Turner, 1968; Benson and Covey, 1974;
Grover, 1977a) show acid herbicides, including 2,4-D, to be "quite
mobile" in the soil. No details regarding these studies were provided.
According to Helling' s classification (which ranks pesticides according to
their mobility), 2,4-D was given a rank of 4, with 5 being the most
mobile class. Surfactants were found to increase the mobility of 2,4-D
(HeUing, 1971b). De Rose (1946) found that 2,4-D moved readily
through greenhouse soil. The NRCC review (1978) cautioned that some
of these laboratory column studies do not allow time for equilibration of
the adsorption /desorption process. However, Norris (1970) found that
adsorption and desorption processes proceeded at roughly equal rates,
attaining equilibrium rapidly within 180 minutes.
In laboratory studies low mobility was found by Crafts (1949) and by
Nutman et al. (1945), although no details are available on these
studies .
Some of the variability in results may be due to formulation. Although
NRCC (1978) states that all salts and esters of 2,4-D will be hydrolyzed
to the acid in moist soil, the potential for leaching does seems to vary
with the form of the herbicide. When Wiese and Davis (1964) applied
2,4-D to columns of silty clay loam soil, it was found that the
alkanolamine salt, which is 100% soluble in water, moved 15 inches,
while the butoxyethanol ester (with a solubility of 16 ppm) leached
3 inches. The lower mobility of the ester forms (as compared to the
salt or acid forms) was confirmed by others (Smith and Ennis, 1953;
Aldrich and Willard, 1952; Barnett et al. , 1967).
The type of soil, particularly the amount of organic matter, may also
account for the variability in results in studies of the mobility of
2,4-D. Ogle and Warren (1954) showed that 2,4-D had low mobility in
muck but leached readily in mineral soils. Hernandez and Warren
(1950) showed that the sodium salt of 2,4-D leached 7.5 cm in a peat
soil and 13 cm in a soil with low organic content after 10 cm of water
had been applied. Several investigators have attempted to correlate soil
11-61
properties with adsorption of 2,4-D; correlation has been found only
with the percentage of organic matter in soil (Hamaker et al. , 1966;
Grover, 1973 and 1977; Grover and Smith, 1974; O'Conner and Ander-
son, 1974; Liu and Cibes-Viade, 1973). Acid herbicides, including
2,4-D, have been found to adsorb readily to soil organic fractions
(Harris and Warren, 1964; Grover and Smith, 1974). Two studies have
shown a high degree of negative correlation between phytotoxicity and
organic matter content of soil (Meadows and Smith, 1949; Upchurch and
Mason, 1962).
The strength of the adsorption of 2,4-D to organic matter is unclear.
On the one hand, two studies have shown that 2,4-D is held tightly to
organic matter; attempts to desorb the herbicide with water have
yielded limited recoveries. (Harris and Warren, 1964; Grover, 1977).
On the other hand, Norris (1970) found that both adsorption and
desorption of 2,4-D were rapid on forest soil material, suggesting a low
energy of adsorption. Support for this idea comes from equilibrium and
kinetic studies done by Hague and Sexton (1968) and by Khan (1973).
These studies found that the interaction of 2,4-D and humic acid was a
relatively weak one, with physical rather than chemical forces holding
the 2,4-D in the interior spaces of the humic acid.
Most investigations show that 2,4-D adsorbs only weakly and in small
amounts to clay particles (Harris and Warren, 1964; Scott and Lutz ,
1971; Grover, 1977; Coffey and Warren, 1969). This is to be expected,
given the anionic nature of most of the dissociated forms of the 2,4-D,
and the negative charge of the surfaces of clay particles. Although
some adsorption can occur at pH levels of 3 or below, 2,4-D adsorption
onto clay at normal soil pH is nil or even negative (Frissel, 1961;
Frissel and Bolt, 1962).
Runoff The few studies available suggest the potential for 2,4-D
movement in runoff may be significant. When 11.2 kg/ha and 1.1
kg/ha of the amine and ester were applied to 16%-17% slopes, the
amounts of the 2,4-D ester collected in the runoff water were 3.4 ppm
11-62
and 2.0 ppm for the two rates of application, respectively. The
amounts of the 2,4-D amine collected in the runoff water were 4.5 pm
and 2.0 ppm (Wilson and Cheng, 1976). In a study using the isooctyl
ester of 2,4-D, Bamett et al. (1967) found that the amount lost
exceeded 10% of the amount applied, and that the highest concentrations
occurred in the first 15 minutes of runoff during a rainstorm. TRW
(1981) suggests that the less water-soluble forms may have more
potential for runoff because of their tendency to be held at the surface
of the soil. The TRW report cites a study by Tarrant and Norris
(1967) in which artificial rain was applied to a test plot of sandy loam
soil. The results showed that 3% of the relatively water-soluble amine
was lost in runoff, while 27% of the less-soluble ester was lost. (This
negative correlation between solubility and runoff is contradicted by the
results of Wilson and Cheng (1976), mentioned above.)
A study by Douglas et al. (1969) showed that untreated strips of
vegetation on either side of water channels could minimize contamination
by 2,4-D.
Persistance /Degradation There is general agreement that 2,4-D can be
considered a non-persistent herbicide (Newman and Thomas, 1950;
Norris, 1966, 1967, 1970; Helling, 1971; NRCC, 1978). It is
extensively degraded (85%-90%) in 15 days in many soils (Freed and
Montgomery, 1963; Hernandez and Warren, 1950; Loos, 1969; Norris,
1966, 1970, 1971).
The half-life of 2,4-D in forest-floor material was found to be 10 days
in a field study (Norris and Moore, 1971) and 4 days in a laboratory
study (Altom and Stritzke, 1973). Longer half-lives (14-41 days) were
found in a study using Saskatchewan soils (Foster and McKercher,
1973). Table 11-15 documents the various studies and the percentages of
the amount applied that remained after a specific length of time.
11-63
o
$-1
o
<n
r— (
1— 1
(U
"»-•
,i4
i-H
N
S
■!->
R]
u
2'
o
C/3
o
'O
^
rH
C
n)
4-»
Cfl
!h
B
0
u
•4-)
(U
•X-
*
nO
'rt
>o
nO
O^
c^
rH
o^
«— '
1— 1
•
«^
1—1
u
(ti
(V]
c^
o
w
^4
u
S
en
(0
C
(«
no
••H
I— I
fa
I
CO
o o
•^ o
^
fO
in
o
bO
un
O
I
HH <^
pa
<
fa
O
U
2
fa
H
w
fa
Oi
. <"
1 -M
nJ oJ
1— t
ac
a, o
C/3
< -^
2
c
o
■4->
I— I
E
o
fa
o
in
nO
2
0)
o
(M
2
4:
(M
Q
2
un
V
•X-
*
Q
2
Q
2
>*
u
^H
g
en
0)
en
fi
<u
0)
•u _
^ -
1— H
1— '
Pu
aj
lU =
fa
u
0
0
w
1— 1
c
E
<
fa
3
0
en
1— 1
Q Q
2 2
bo
^
CTJ
OJ
:>-
^
^^£
•
"■***
•
in
bO
in bO
r— 1
X
r^ X
4)
«k
•^
•> rf
S
00
•
•
1— 1
00 .
• 1— (
03
cn
en
cn cn
c^
ro
r~ fo
2
2 2
3:
^H
- ^
w <u
OJ tl
tn
,-1 <u
^_^
5h u
CU 0
0 0
cn cn
(— ( (—1
CO
2
I
0)
T3
H cn
^
rt
J
*
cn
2
cn
2
cn
(U ,-H
p-H
^H rt
•i-t
0 T
0
m Sh
cn
1— 1
(U
a
H
•rH
0
cn
cn
alder
r mat
E
0
1 — 1
HJ
0
t><
•f-H
u
T3 0
0
cn
£
0) cz;
1— t
cn
o
u
•1-1
fa
cn
2
cn
2
a
>
0
J3
-t->
OJ
c
•1-1
u
0
0
a.
■<->
bfi
CTJ
C
»^
cn
^->
1— ^
^H
• r-t
• 1-H
0
^
cn
2
• fH
fa
bo
C
.pH
^M
(T3
(U
«k
r—t
p— I
0
•l-(
0
cn
cn
TJ
<
0
<4H
(Q
0)
CO
o
cn
cn
"^ o
.1^ (U -
(U " Vh
w c ^
II rt
.« '-' cr;
^ 2 *
2 * *
* * -it
(U
u
u
o
»4
00
(M
u
vO
c
»4
O^
rt
V
0)
f-H
h
U^
^-^
^-v
0
n3
•
2
1— 1
o
C
a>
rt
ffj
>^
(«
Si
(U
0)
0)
en
o
en
(A
o
Sh
p^
n
V4
d
<u
(U
o
fa
CQ
Q
t^
2
rH
•^
1
sD
O^ CO
o
CO
o o Ln
1
in
T^r CT^
?
rH (M CO
^
^ o
H
1^
2
'^
O
U
"N^
b
o
in
1
W
1
1— 1
o
M
2
m
Cx]
J
H
(23
cn
<
H
PCJ
w
PU
(30
tlO
o
E
lica-
Rate
App]
tion
o
■t-»
I— I
a
o
fa
o
cn
2
Q
2
bO
Q Q
2 2
00-
un o • rs]
<Na cn ID (va
in
<N3
CO
2
LTl vO u^
in I-*
CO
2
cn
cn
cn
cn
cn
2
2
2
2
2
O
(0
3
o
o
03
tn
■«-»'
c
<V
>^
<U
J3
fd
^
rt
u
o
cn
cn
cn
cn
J
O
tn
OJ
2
2
i
T3
cn
o
cn
C
rt
^
0)
(U
a
^
>>
a
■t-»
H
OJ
^
1— *
•1-4
cn
0
(«
cn
cn
cn
2
13
T3
U
(U
^ cn
cn
2
cn
o
u
13
r-H
13
•i-t
a
u
o
o
.2J S
13
c
o
2
o
a.
cn
o
2
(
cn
2
Q
2
*
Degradation of 2,4-D is predominantly microbial, rather than chemical,
and numerous bacteria have been isolated that are capable of degrading
2,4-D. Some of the these are listed in Table 11-16, along with the
identified reaction products. The degradation of 2,4-D has been well
studied and can be roughly summarized in the following steps:
1. Esters and amide formulations are first hydrolized by an enzymatic
or a soil-catalyzed reaction (Norton, 1975; Smith, 1972).
2. The acetic acid side-chain is removed to yield the corresponding
phenol.
3. A ring cleavage results in an aliphatic acid (TRW, 1981; NRCC,
1978; USDA, 1973).
Aliphatic acids (e.g., succinic acids) are common soil constitutents
which microorganisms can use as carbon sources, thereby releasing the
original material as CO..
Volatilization Little information was found on the potential for loss of
2,4-D by volatilization from the soil surface, even though some forms of
the herbicide are highly volatile. Based on limited data, TRW (1981)
suggested that volatility may affect the rate of initial loss but that it
would have an insignificant effect on long-term persistence.
Persistence in Water Several monitoring studies have investigated
residues of 2,4-D primarily from agricultural areas. In a survey of 20
rivers in the western United States, the U.S. Geological Survey found
40 of 331 water samples to contain 2,4-D in concentrations of 0.03 to
0.35 mg/1 (Manigold and Schulze, 1969). Considerably lower
concentrations were found in water from eight agricultural watersheds
in Ontario: 2,4-D was present in 39% of these samples, with a mean
concentration of 0.2 yg/l, with a range of <0.1-16 yg/l (Frank et al. ,
1978). These same investigators studied 11 agricultural mini-watersheds
and found that 38 of 404 samples (9.4 %) contained 2,4-D. Although in
most samples (33 of the 38) the residual level was less than 1 yg/1, one
contained 16 ug/l and another 320 yg/1. The investigators explained
the very high concentration as the result of spraying a nearby right-
of-way at the time of sampling. Other information on residues is pre-
sented in Table 11-17.
11-66
en
o
C
0)
u
.*00
^^ ir>
m»
o o-
<«^
vO I"*
irt
cr-
^
1—1 •
o^
>-^t>
i-t
r- iC
s^
in M <^
(19'
d
lorri
r (1
962)
f 1 ^r
"^
zgerald (1966)
II
!— 1
•
■4->
cn
0
udus (1950); Bell
)60); Faulkner an(
oodcock (1964); ^
teenson and Walke
ay lor and Wain (1
ulkner and Wood<
wcett et al. (195
vD
<—{
•
t— 1
cn
o
cn
fa
'0
>>
■4->
o
a nJ
o
fa
J
< ,-( :5 cn H
fa fa
J
<
^
CQ
<
c/3
cn
<
O
o
o
u
CQ
Q
I
CM
fa
O
O
t-H
H
<
P
<
O
Q
01
u
O
U
o
+j
u
u
(U
c
o
c
o
o
3 (U
o a 4^
^ u
>> o
y
o
C
o
S
T3
O
0-
S
o
u
0)
O
U
O
1—1
C
•1-1
o
I— I
c
3
o
3
>_^
T3
-0
^
o
o
,.H
0
01
rt
o
u
Q
c
(U
u
o
1
0)
0
0
o
c
0
o
1
0
2
3
E
3
e
0)
o
0
0
ec:
u
o
1-H
O
f—H
T3
u
• rH
T3
c
X
^
>>
1
.1-1
o
o
Si
"^
(T3
1
1
1
•^
2
ca
a
o
(M
c
c
I
>^
o
o
O
I— I
u
I
05 T3
o 53
I
o
I o
in '.-I
I
O
a;
u
>>
><
o
c
*^
CM CU
o
c
a
o
;h
o
l-H
^ 0)
-2
• o
^ 1—1
*^
<u
cn
l-H
o
,c
o
u
1— t
>
cn
T3
o
PC5 O
0
cn
C
(N3
(ti
»4
T3
0
<0
l-H
M
X
>^
0
• 1-1
'0
-0
u
13
CO
>>
(Nl
3:
(fl
04
(fl
U)
«}
C
g
cn
0
0)
T3
u
3
(U
(U
a
cn
cn
Cl^
Pu
cn
o.
■»-»
a
0
cn
rt
^
(fl
0
E
0
a
}h
u
rC
0
0
z
<
CO
?=!
•tH
dot
aj
cn
•
S
a
3
CO
• rH
;m
■♦-»
a
0
u
•§
u
!>^
rC
u
•M
0
<
0
u
o
CO
00
00
c»-
r-
CT^
o
t-i
1—1
«X"-S
\^
^_^
^3 ^
•
•
C OS
t-H
rt rH
OJ
H
^t^^
T3
+J
■4^
nJ N
<U
(U
0 ^
dc-;;
pi^
^
S
(4
nj o
;h
h
2 CD
pL,
(x<
(0
•rH
o
CO
l-H
CO
■♦->
C
<u
S
S
o
U
o
en B
0) .
■-U (J 4^
cn
,5 rt
C >> O
^ s^ nj
3 a. lu
c/3 +j iD w en
.PH ^O
S C
<« o
CO TJ
■♦->
en
c
o
s
en ;^ '^r
Pi
Q
I
o
CO
Ui
D
Q
I— I
w
w
05
° i:
(U (U
GO ^
CQ
(U
a
M
E
Q
w
•1-<
1
CtJ
-^
M-l
•♦->
*
0
o
(M
•
o
o
2
SH
cn
0
p— 1
a
•
0
a
Z
r/1
(30
a
&0
^»
c
P.
bO
0
in
3.
PH
CO
sO
4->
•
o
1
•
f— 1
1
O
fM
CO
■(->
1
CO
l-H
1
o
•
•
o
V
f— (
V
o
CO
CO
CO
00
CO
o
00
<M
I
&0
3.
CsJ
fV3
00
I
^ .(
03
0)
<
• pH
s
03
CO
>
2
w
C!
u
cn
CO
-0
o
«k
pfl
cn
CO
$H
03
cn
0)
fi
+->
•PH
E
• o
o
U •f-i
■ p-4
•r >^
u
5h (t3
ttO
bO-M
<
o
l-H
CO
t—i
o
03
■f->
c
o
>
•pH
Pi
c
03
o
03
cn
c/2
cn Qi
(U cn
1=3 cn
p^ (y
> C
^£
a
CO
y
u
o
B
o
-a
c
e
en
p-
1-1
I
o
CX4
4->
CO
_ 00 E
■•-»
2 c S-
•r' ex
X
s
-a :3
!h >^
-M
e
•55 e
3 cd rr
lU
0
pi.S
^ D- •
0)
O
(i Cfl o
en
(0
•rH
;h
o
2
I
0}
u
o
CO ^ ;5
to
O oj fO
rt
^
0
.r<
-^
Ul ^
M
2 P
TD
i-t
C
*^
ctf
(0
C -^
•c
^^
00
Vi
P o=^
c
0
i:: -H
;=: ^
2
CQ w
o-e .S
£ 2 1 >^
ffj Sh 1 rt
^ V
03 -S rt ^^
(U C 0)
&0
C k"
> ■ ■
c
3 rt !
u5 ^ <" t«
0
o
0 «
C 1— t K>»
en
■*j
C ^ u]
• r-l
G
0 ^ p,'^
0
0 3 ^Jjv,
Q a. tn r-H
vO
a
Z 'V '<**
p:J
^_^
W
Q
H
W
<
o
1 ^
3
^
srf
§•2
2
D
HH
2
00
O 4->
H
2
O
Q
1
OJ
Pi
0 jh
O
r^
1—1
tL.
1
o
CO
t— t
Q}
t-H
en
1— <
a
s
00
J
D
c ^
CQ
Q
cn
:si
<
HH
H
cn
0
(ii
•
o
o
o
2
No. of
Samples
00
00
E
00
•
oo
in
I
CM
00
3.
nO
00
e—H
S
00
•^
E
00
•
<N1
o
r— 1
1
1
1— 1
ro
o
o
o\« dP
OO O^
00
E
p-
o
1
vD
P-
O
B
o
V
Q
2
I
CO
>>
13
0
^
rt
<U
^4
U
(U
<
00
^
• rH
C
f— 1
• rH
a
si
T3
3
cn
2
o
cn
T3
C
O
a
E
u
a
4->
c
-4->
cn
c
o
(U
o
u
00
c
o
lU
• IH
M-l
o
cn
c
1— »
•l-l
M-l
(U
cn
E
0
cn
E
oJ
oJ
<U
<u
^4
}h
^
Oj
fa
cn
OJ
cn
cn
E
E
rt
(U
(U
Si
V4
•*-»
-t-"
cn
cn
C
cn
o
•
00
p
<u
u
O
(U
c
••->
^
cn
(U
(U
cn
^
(U
rH
^
*-l
I
0)
u
O
W
J3 O^
rt
•«:l^
13
C
l—i
CO
-•m^
N
c
■4->
1— 1
o
3
e
X
u
y
«J
c/3 X
o
nt
0)
in
CO
4)
a
s
o
O
I
3 ^
^ rH > W
^ c Jh C
rt 3 (u o ^
bO
en
•4-)
C
C rt
0)
;=: ^
E
rt
(^^ s^
4-»
$-1
w
W r-H rt
+J
u
o
w E u
7 i s
i 5 2 J
rg T3 MH Cl,
0)
o
u
Q
U
2
I— I
I
W
2
O
O
O
w
M
D
Q
I— I
w
<u 0) .2
!= S 2
ex; o ^
CO
^
bO
'a.
c
E
Q
1
W
•1^
0
C
O
(NJ
0
y
2
Q
2
U)
f-H
^
00
E ;.
St3
a
r-\ E
1— 1
o
' C
c» .S
o
? ^
1
1 -rH
o
IT)
o
o
Xi
• ft
bO
• 1-H
I— H
bO
a;
2
i2
O Q,
O
oo o
I— ( •^
o
I
<+-!
01
0
0)
1— H
a
0
S
2
(U
bol
c
■ 1-1
S
rt
(tJ
'rt
2
0
l-H
u
-C
fa
)m
o
^•^
0)
a>
0)
^
bo
s
03
D
.1^
X
■+-1
u
0
(U
<u
J (^
Oi
RJ
-C
.1-1
V4
OJ
•i-i
E
bO
c
O
• fH
O
cn
'O
•k
C
u
o
3
a
0
cn
(U
w
c
"^^
o
(d
tlO
<d
C
'? ID
CO
03
o
2
03
Once present in the water, 2,4-D may be detectable for 3 weeks to 4
months (Schultz and Harmon, 1974; Wojtalik et al. , 1971; Frank and
Comes, 1967). Microbial degradation does not appear to be significant
in most waters (TRW, 1981; NRCC, 1978), unless the system is warm,
aerobic, 2,4-D-rich, and nutrient-rich (Halter, 1980). These conditions
are not typical of most natural surface waters in Massachusetts. No
breakdown of 2,4-D occurred in lake waters aerobically incubated in the
laboratory for 120 days (Aly and Faust, 1964). Watson (1977) and
Schwartz (1967). Both documented that 2,4-D is stable in water for up
to 6 months, depending on the microorganisms present, nutrient levels,
and amount of suspended sediments.
Chemical hydrolysis rates vary considerably with the form of 2,4-D. At
pH 6, the hydrolysis half-lives range from 26 to 220 days for several of
the esters at 25° C (Zepp, 1975). For some forms of 2,4-D,
volatilization may be more important than hydrolysis at pH 6. Half-lives
for vaporization at pH 6. Half-lives for vaporization of the butyl,
octyl, and methyl esters are 1.1, 11.5, and 21.7 days, respectively.
Some photodecomposition of 2,4-D may take place at the surface of
water, although it is minimized in well-mixed deep ecosystems (Zepp et
al. , 1975; Leighton, 1961). Adsorption onto the suspended particles a
does not appear to be a significant removal mechanism, according to a
review by Halter (1980).
Indicators of Potential Ground Water Contamination
Table 11-18 provides information on parameters associated with the
mobility of 2,4-D. These parameters, and their associated thresholds,
have been suggested by EPA for use in assessing the potential for
pesticide contamination of ground water. A discussion of these para-
meters and thresholds, and the methods for arriving at designated
values for individual herbicides, is presented in the main body of the
report as part of the discussion of the fate of herbicides in the
environment.
11-71
TABLE 11-18
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION
2,4-D
Indicator
Solubility
K
oc
Speciation at pH 5
Hydrolysis hedf-life
Photolysis half-life
Vapor pressure
Value for 2,4-D
Insoluble to
infinitely soluble,
depending on form
66-307
Anionic
Rapid to slow,
depending on form
16-29 days*
6.0 X 10 mm
Hg at 25"C
Threshold
>30 ppm
<300-500
Anionic
(negatively charged)
>6 months
>3 days
-2
<10 mm Hg
* For dechlorination of the ester.
11-72
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Except for one study on reproduction, a number of tests show 2,4-D to
be non-toxic to test birds. Heath et al. (1972) and Hill et al. (1975)
reported LC_- values for mallard ducks, bobwhite quail, Japanese quail,
and pheasants to be >5000 ppm for 2,4-D acetamide, butoxyethanol
ester, and dimethylamine salt. Tucker and Crabtree (1970) reported
LD_- values that ranged from >>100 mg/kg to approximately 2000 mg/kg
for mallard ducks exposed to 2,4-D technical acid, technical sodium
salt, and 4 lb acid equivalent /gallon of amine. These data are
summarized in Table 11-19.
Studies by Somers et al. (1972, 1974a, b, c) reported that spraying
eggs with 2,4-D and 2,4,5-T, alone and together, resulted in no
adverse effects on hatching chicks or embryos. An additional study by
Kopischke (1972) found no significant effect of 2,4-D on the hatch-
ability of pheasant eggs.
Two studies by Hilbig et al. (1976a, b) found that spraying eggs of
quail, pheasants, and chickens with 2,4-D, in concentrations up to 10
times the recommended doses, produced no effect on the hatching rate,
body weight, sexual differentiation, reproductive performance (as
adults), or number of malformed chicks. On the other hand, in a
study by Lutz-Ostertag and Lutz (1970) which investigated the effects
of spraying 2,4-D amine at a concentration of 1.1 kg a.i./ha on fertile
eggs (in an artificial nest) , they found 77% of the ring-necked
pheasant, 43% of the red partridge, and 77% of the grey partridge
embryos were dead on the nineteenth day of incubation. Surviving
embryos were malformed or partially or completely paralyzed.
Fish
Although toxicity varies with formulation and environmental conditions,
DeVaney (1968) concludes that many of the formulations (especially the
esters) are toxic to fish. Halter (1980) showed that the acute toxicity
of 2,4-D to fish varied considerably, depending on the species of fish,
the water quality, and the 2,4-D formulation. A study by Woodward and
11-73
en
Q
p:i
h-i
CQ
O
o^
H
r— 1
1
P
1— t
1
1— (
■^
w
J
CQ
[n
<
o
H
>^
H
h-l
u
1— 1
X
o
H
o
»-•
o
en
S
en
p:5
H
C
.2
■♦J
a
s
o
in
in
in
in
r-
p«-
c»-
c^
o^
o^
CT-
a^
i-H
1-1
fH
t-^
o-x
^-^
^—^
^-^
•
•
•
•
1— 1
1—1
I— 1
1— 1
n]
(ti
(4
a
•M
•*■>
■M
•M
V
9i
(U
(U
f-H
f-H
f— 1
/— V
rH
^_^
:3
1— <
•i-i
•IH
0
1— 1
0
K
X
E
E
T3
TS
73
r-i
T3
1-^
i::
c
C!
C
(ti
oi
at
0
03
0)
^«— %
^••■•v
i^-*K
J*"'^^
^1*— s
<^**«fc
y«"V
^•"^
^""^
!h
y>>.
(('•■V
^*"*K
;h
(Nl
(M
ra
(Nl
(N]
rvj
CO
rj
(VI
+->
(VJ
<N]
(Nl
■4->
r~
r-
c^
r-
r^
r-
c^
r-
r^
J2
r>-
r~
c-
^
CT^
o^
o^
o^
o^
o^
cr-
0^
cr^
03
0^
0^
0^
CO
1— 1
1— I
i-H
rH
rH
1— t
r— 1
rH
I— 1
^H
rH
i—{
l—<
^
•
1— H
•
l-H
p— I
•
I— I
•
1—1
•
1—1
•
1—t
•
I— <
•
i-H
0
•
1—1
•
rH
•
u
T3
rt
nJ
rt
rt
rt
OJ
n
nJ
OJ
c
oJ
03
'rt
C
•»->
■»-»
+j
■^
4->
■fj
•t-»
■+->
•t->
OJ
-M
•4->
■«H
03
(U
lU
(U
(U
(U
a;
<u
0)
(U
;h
0)
a;
<u
^
X
^
^
^
^
4:
^
4:
^
0)
JC
^
^
OJ
-4^
•*->
4->
4->
■^
■M
-♦->
■♦->
■4->
4-»
•<->
■fj
OS
03
CB
rt
nJ
rt
rt
03
OJ
y
03
05
03
0
(U
<U
(U
0)
(U
0)
<U
0)
<U
3
0)
S
_QJ
3
E
X
X
E
K
E
E
X
E
H
(J-i
1-4-1
X
H
o
o
o
IT)
A
O
in
(tj
3
cr
V
•♦->
en
• IH
<u
^
•r<
0
^
(U
^
a
0
w
CQ
0
0
ro
0
r^
\r\
■*
A
0
0
LO
in
Q
U
J
J
CM
<
W
<
U
<
H W
2
w
2
u
2
<
< aa
Q
<
P3
Q
<
CQ
Q
H
cr
en
0)
ni
(0
(4
0)
(1^
u
U
»— I
I— I
o
o
rH
A
A
in
ro
o
{N3
A
A
O
o
o
(M
e
o
in
Q
in
W < ^^ cn o
W S < cn <;
< OQ Q H H '^r
<
C
OS
CO
03
(I4
00
OS
<u
C
E
4:
-t->
<u
E
0)
1
c
"IS
>
• iH
cr
5 £
Q
fO
^4
■♦->
(A
0)
'o
c
OS
■*->
(U
X
o
p
vO
03
en
o
en
'c3
o
c
u
a;
H
cu
(Nl
in
-a
:i -13
03
(U
o
03
(A
Q
fi
1
0
•^
Oi
•>
t:u)
(SJ
u
03
OS
O
• IH
c
o
H
I
• r^
o
03
Mayer (1978) showed the effect of temperature on the toxicity of 2,4-D
to fish (Table 11-20) . The data suggest that toxicity increases as the
temperature decreases. The authors concluded that neither water
hardness nor pH significantly influences toxicity. A study by Schultz
(1973), however, suggested that channel catfish and bluegill accumu-
lated more 2,4-D at pH 6 than at pH 9.
It has been observed by several studies that the butyl ester
formulations of 2,4-D were many times more toxic than the
corresponding acids. Cameron and Anderson (1977) noted that in the
field the esters were quickly hydrolyzed to the acid or salt. Cope
(1965) noted delays in the spawning of bluegill sunfish for periods of
up to 2 weeks after treatment with propylene glycol butyl ether ester
(PGBEE) at 5 and 10 ppm. No effects on reproduction or survival of
fry were noted.
14
A study by Schultz (1973) reported that C-labeled dimethylamine salt
of 2,4-D, at concentrations of 0.5, 1.0, and 2.0 mg/1, produced no
mortality or adverse biological effects. It was found that 90% of the
residues in the muscles of bluegill exposed to 2.0 mg/1 were composed
of metabolites of 2,4-D. In studies by Sikka et al. (1977), and by
Stalling and Huckins (1978), it was suspected that decomposition of
2,4-D had occurred in the water due to microbial action.
Lower Aquatic Organisms
Two studies investigated the effect of 2,4-D on amphibians. Sanders
(1970a) determined the LC^. values for 24-hr and 96-hr tests on
bU
Pseudoacris triseriata to be 100 mg/1. Cooke (1972) found that 50 mg/1
of 2,4-D produced no visible changes or behavioral abnormalities in
tadpoles of Rana temporaria.
Elder et al. (1970) found that 2,4-D exhibited low toxicities to all fresh
water and marine algal species tested, at concentrations of maximum
solubility in water. Hawxby et al. (1977) found no adverse effects on
cyanobacteria and algae tested at 0.10 to 10.0 yM (Anabaena variabilis,
11-75
i
3:
in
1— (
fa
O
H
o
(N3
Q
1— 1
1
w
(VJ
J
fa
<
O
H
>^
H
1— 1
O
t— 1
X
o
H
u
)-■
0)
>
rt
Cil
2
■(-»
T3
O
C
c
OJ
(U
T3
0)
u
T3
•
u
TJ
^
3
O
3
0
O
Q-
W
^
(U
u
C
(U
-d
^-^
0
■4-»
o
•
U
E
1
o\o
J
o
in
ro
^
o^
•
d
^^
en
^,^
Pi
S
o
•
■^
o
•
wn
o
J
u
(U
^
S
1
u
o
04
S
a>
H
o
• rH
«J
l-H
E
O
fa
in
rs]
,— »
^-^
<.— «.
o
^—^
in
X— s
^—^
x-^
/"-s
o
o
<V3
■"^
o
00
vO
o
o
r^
ro
i-H
■"a*
o
O
CM
1— 1
vD
(NJ
•^
r^
fO
00
vO
o^
vO
•
o^
•
C^
<T>
r-
C^
•
•
1
•
1
•
1
f— 1
1
•
1
1
1— 1
•
1
•
1
•
1
•
1
r— t
1
o
c^
o
o
CO
■^
CT-
in
r— 1
(Nl
■^
vO
lD
o
(VJ
o
in
sO
f— 1
CO
•^
(Nl
•
•
•
•
•
vO
•
in
•
•
•
in
•
00
•
o o o o o o
•^ r- CT^ CO oo o
LO c^ T^ o r- vO
o o o o o
"^ (n: o CO o
sO 00 r- vO o
in to
un
m
m ID
in
CO
Vi
.1-1
>
nJ
Q
T3
C
(0
(U
(VJ (VJ
■I
>
bO =
o
CO
W
O
CO
(Nl
fa
CQ
fa
PQ
a
CO CO
I
CO
W in
fa fa ^cj -^, ,
« W " W
O CQ ^
3
0
^
■4->
•4->
(«
rn
0
1)
$1
•d
^
u
■*->
(U
4->
a
3
m
U
O
bO
a;
S
u
u
o
o
73
Q
(
y^
vD
O^
vO
O
O^
cr>
t— 1
f— 1
>•»•
lU
0
o
1— ;
«J
<
J
ffi
cn
1-4
t>4
o
H
o
1
Q
■ 1
1— 1
1
W
(M
J
CX4
<
o
H
>
H
t-i
O
1— 1
X
o
H
3
6
a
o
O
O
o
a;
H
C
o
•i-i
■*-»
o
CX4
(M
CO
(U
a
in
1
1
00
1
O
O
u
w
in
r-
a
W
<
CQ
H
2
O
CQ
Q
^
Sh
o
0
^
+J
;h
0
3
0)
c
o
+J
c
»4
0)
.1-1
•t->
4:
S
^
(TJ
73
0
^
rt
^
0
<u
fl
^
^
.1-1
CO
•^
cfl
nJ
nJ
^
ffi
fa
s
QU
B
0
w
•^
(U
X
4.J
.1^
4:
^
4-»
a;
•§
13
f-H
■i-<
lU
>>
s
C
-t-»
(4
(U
D
u
■M
0
^
<
CO
'0
u
^
^
•
'go
01
0)
<u
1—1
^
l-H
>>
>>
a
• «k
+->
0
(M
3
u
•
^
a
r^
II
1
P
1
n:
1
1
a
rg
(M
Cvl CO
Lyngbya sp . , Chlorococcum sp . , and Chlorella pyrenoidosa) . They also
concluded that 2,4-D was toxic to lower aquatic organisms (TL^.. = 0.1
to 2.6 ppm) except crayfish.
Many studies have been done to assess the effects of 2,4-D on lower
aquatic organisms (Table 11-21). The data suggest that toxicity varies
with the different formulations of 2,4-D. Rawles (1965) noted that
when 2,4-D acetamide was applied at 20 lb /acre to control Eurasian
milfoil, it was toxic to blue crabs and eastern oysters. Butyl or iso-
octyl esters were not toxic to these test animals. The isooctyl toxicities
of the different formulations of 2,4-D were also investigated by Sanders
(1969, 1970b) and Zimakowska (1973). They concluded that some of the
ester formulations were the most toxic.
Indirect Effects on the Aquatic Ecosystem
After an extensive review of literature, the NRCC (1978) concluded that
spraying of phenoxy herbicides, including 2,4-D, to control nearby
terrestrial plants may cause direct lethal or sublethal effects in fish or
aquatic invertebrates. If the concentration is sublethal but high enough
to kill aquatic macrophytes, a complex series of secondary changes may
occur throughout the ecosystem, resulting in reduced oxygen and pH
levels, increased CO- levels, and changes in the species composition of
invertebrates and phytoplankton. In response to these changes, a
number of food webs that they were part of would necessarily be
affected.
Mammalian Wildlife
The effects of 2,4-D on mammalian wildlife have been the subject of a
number of studies. Shifts in the population size of pocket gophers
after spraying with 2,4-D have been reviewed by Tietjen (1973).
Johnson and Hansen (1969) studied the effects of range treatment with
2,4-D and the effect on mice, chipmunk, and vole populations. Wilber
(1963) followed the effects that spraying 2,4-D esters had on grazing
by elk for several years. Deer forage was followed for 6 years after
treatment with 2,4-D ethyl ester in a study by Krefting and Hansen
(1969).
11-78
i
ca
in
%o
o^
D
u
1— t
13
•M
0
p
W
CQ
o
(0
0)
C
^ X
(N3
I
CQ
<
m
<
O
o
o
l-H
H
<
a
<
o
o
o
H
H-l
o
X
o
C
o
■1-1
•♦->
Q
E
o
fa
o
en
o
to
C
0
(U
■«->
^H
o
o
(U
(U
<+-(
a;
T3
M-1
^H
o\o
0
"-M
o
w
LD
<i
^^
(U S
ir>
tfi a
r>-
y a
•
U — '
ro
(Nl
o
V4
o
CUO (20
en en
a;
en
-0
en
oJ
y
^3
00 O^
CO CO
if)
en
en
>>
I— I
03
U
03
a
o
a 03
o
o
S
u
o
S
I— I CNj ro
O
en
en
OJ
u
u
o\o o\« o\«>
O o O (T-
Z r— I r-l CO
0)
E
J o
H 2
<u <u
o
z
m
ir>
in
o
o o
0) C ceJ o3
X O X ><
•i-t t! •'"' ••-•
03
<N3 X
CO ro
o
o
en
OS
u
o
<u
iG O O
O U
o c c
(J .-^ .1-1
u
VM
o
2
0}
en
03
u
o
a)
-a
en
03
U
lU
T3
o o
ir» if>
(va in
t
u
u
»4
>>4
u
;h
X
X
^
^
^
X
1
s
S
£
1
ZZ
S
1
1
S
S
SI
1
1
vO
00
vD
00
■<^
=
s:
00
0^
•^
O^
'^^
'*
w
u
ti
W
w
^^ CO
w
w
w
U
w ^
^ < W
CQ
<
w
CQ
<
W CQ
<
U CQ
CQ W
W 2 E
CJ
w
:§
n:
0
a
2
3: 0
w
2
a: a
0 C^J
qa Q W
cu
pa
Q
w
Qa
CQ
Q
W (^
CQ
Q
W (1^
cu cQ
en
c
OJ
o
en
>^
O
a
E
•1-1
u
X
X
CO
C
o
c
03
o
•4->
X
u
<
0)
u
u
o
03
00
o
CT^
i-H
v^
(U
a
^-^
0
(Nl
O
C^
rH
T3
03
>>
cn
<u
u
l^J ~
<u
o
T3
C
C
•i^
rt
X
C/3
Q
O
2
l-H
H
2
O
O
I
CQ
<
01
:2
o:
I— I
2
<
a
o
o
H
<
a
<
O
J
o
H
Q
I
o
>^
H
I— I
U
(—1
o
o
M-l
C
o
oJ
;^
Q
S
u
o
E
c
U
O
o
o
o
o
o
o
in
LD
in
in
in
in
J
J
J
J
J
J
H
H
H
H
H
H
a> E
w a
9 a
ro
(M
o
o
•
•
o
o
Q ^-^
(M
cn
1— 1
(— 1
o
03
in
oooooooo
inininmininmin
ooouoooo
no in in
rH 00 00
u
I
u
1
(NJ
CO
«
c
>^
X
nS
a
U
rt
U
Q
c
o
+->
03
00 nO
I
QO
u
I
w
u
W
w
w
W
CQ
w
CQ
w
CQ
U
W
U
w
w
a
w
O
w
O
W
W
W
W
u
w
a.
pa
CU
CQ
CU
PQ
CQ
PQ
ca
03
P3
in
U
1
Q
I
(Nl
In
o
a
H
o
00
I
u
Xi
I
00
X,
I
u
CO
(A
•4-»
X
(U
U
•M
CO
!U
0
l-H
0
G
>^
c
• 1-t
1-^
E
01
bO
03
X
rn
f-H
d)
0)
a;
J2
^
C
1— 1
-M
J 1
1— H
X
>>
<u
>>
>^
0
•(->
3
E
4:
■«->
0
■4-)
3
X TJ
a;
CUX
Q Q Q Q
Q
■^
tT
Tj*
•^
"^
(M
(M
00
CM
Cs]
i—t ro CO ^ in
In a review of these studies, NRCC (1978) concluded that the
applications did not reach toxic levels for any of these species, and
that the effect on vegetation resulted in an increase in food availability
for voles, elk, and deer, and a decrease in the food source and cover
for gophers and chipmunks. The populations of voles, elk, and deer
increased in size, but populations of gophers and chipmunk decreased
in size. The population of mice remained relatively stable, probably
due to their variable diet.
Palmer and Redeleff (1969) report that the acid of 2,4-D fed to mule
deer for 30 days at 86 and 240 mg/kg/day produced only minor
symptoms and no weight loss. Tucker and Crabtree (1970) report an
LD of 400-800 mg/kg of the 2,4-D acid for mule deer.
Livestock
Livestock do not appear to be sensitive to 2,4-D (Table 11-22). In a
review of the literature, NRCC (1978) also concluded that there was
little direct hazard of toxicity to livestock, but went on to suggest that
deaths of domestic animals may be linked to changes in plant chemistry
due to treatment with the herbicides. Frank and Grigsby (1957) and
Buck et al. (1961) have reported variable effects of 2,4-D on the
nitrate concentration of various plants. Nitrate poisoning of livestock
has been reported by Fertig (1953). Nitrate accumulation appeared to
be species-specific: some species increased while others decreased
their nitrate concentration. Phenoxy herbicides (including 2,4-D) may
also be associated with increases in the alkaloid and hydrogen cyanide
concentration of some plants (Swanson and Shaw, 1954; Lynn and
Barrens, 1952; and Willard, 1950). In their review, NRCC (1978)
concluded that the significance of any chemical changes and their
potential risk to domestic animals was difficult to assess because the
data were sometimes contradictory or incomplete, and often inconclusive.
Insect Predators and Parasites
The only study presently available is a study by Adams (1960) in which
coccineUid larvae were treated with 2,4-D amine. A four-fold increase
A
11-81
nO
nO
cr-
(— 1
(U
c
h
w
'^
c
«J
T3
fi
<u
3
I-H
3
o
o
•T-n
w
ca
o^
o^
vO
sD
o^
^_^
O^
Nail'
in
t— 1
(4H
f^
>4H
«M
MH
0)
"*^
0)
i-H
l-H
0)
U]
(U
-d
^_^
rt
'O
OJ
r— 1
s
rt
Cr5 =
C^
>>
Pi
t3
(3
13
^4
»— 1
C
a
u
o
C
<0
0)
S
0)
a
•i-t
a
1— 1
.— 1
Ri
0
rt
Oi
04
A
O.
■t->
<u
E
•11
PU
U
O
H
>
u
0 ..
0 <u
w
c
E o
nj
0 c
^
O OJ
■«->
--P
(U
0
C
fl
a tJ
o
•i-i
0 .rH
2
2
cn x>
■M .
O
-I
p rt
GO "^
73
o
}h
cn
en
o
u
bO
O
C
O
E
u
o
G
N
I
0
u
o
&o^
ao lu
W ^ n3
C
o
.1-1
o
C
o
2
u
a;
VH
a> _
o
2
J3
00
• rl
o
u
u
c in
O rt Q O
2 DO J 2
0)
o
2
tSO
O
^->
o
0) (U
o
2
CM
I
CQ
<
O
H
Q
I
fa
o
H
l-H
o
I— I
o
C
o
■*-»
Q
o
Q
en
(U
en
en
0
A
CO
TJ
0
O
o
T3
r— 1
E
m 00
>^
rt
73
C
•p-t
CO
,i*5
E
GO _
E '
o ^
o
o a)
Ln
in M-4
o
.|-H
O "o t)
E "^ 3
O hn en 13
^ r-^ ?
GO
GO
P ^ (va 0)
a
o ^
en
<u
en
o
GO
GO
a
o
in
en
00
13
GO
X
00
E
o
o
en
OJ
Xi
GO
en
03
OJ
73
GO
GO
2P E
o
tn
o
o
GO
GO
E
LD
I
O
00
m
CO
oi
13
oo
03
13
GO
GO
E
o
o
en en
>> >>
OS 03
T3 13
OS
13
00
GO
E
o
o
03
13
GO
GO
E
o
(N]
00
I
03
E
•I-t
<
C
o
•1-1
+•>
OS
E
u
o
fa
a;
c
CO
0)
E
03
'o
c
OS
• IH
H
C
u
•1H
CO
a;
$1
a
9)
4^
a
(Q
(ti
V
T-H
o
l-H
c
>^
0$
3
l-H
CQ
<
c
u
U U
03 ,C X
u
.^ ^
X
03 JZ
CO
U U
-0
>^
CO
I— 1
OJ
GO
»4
(U
0)
c
^
(U
■«->
f— 1
a;
>^
1— 1
a
>^
o
u
3
cu
03
vO
•^
o^
1— 1
•
i-H
CTJ
**
0)
1— 1
(U
1— 1
(U
u
-C
:j
0
.I-H
w
2
in
CO
S
>^
X
0)
O
pc5
Q
2
2
O
O
(VI
CM
I
<
u
o
H
>
O
H
I
o
>^
H
O
(— t
X
o
o
.1-4
u
Q
0)
o
Q
E
•i-t
o
.I.H
1—1
s
o
> ON r-
3 o
(fl
CO
Jh en
>^ o
>>b'0
CO
O r-H
o
nJ Td
en
a;
o
>
o
^ "Jit
< ^
en
-t->
o
o
B
o
en
■»->
<u
(U
V4
O
S
o
o o
2 Z
en
CO
en
en
>^
>s
>^
>'
(tJ
rtJ
rt
nJ
-0
n3
13
^3
o
in
>.
>^
>^
>>
(d
(i
a
rt
2
T3
T3
'O
■ — ,
— .
■ —
afi
bO
(:0
bo
ao
^
^
^
1^
^
• — .
-~~
"— ~
ao
"ab
dO
00
ao
s
a
£
S
e
o
o
o
o
o
ro
tn
in
o
o
"^
(M
rj
r-i
r-i
i-H
s
a
a
<u
X
^
0)
4)
4->
u
■^
0)
0)
+J
• pH
03
^
^
rt
rd
o
w
W
u
o
U
o
+*
u
CO
(U
o
•4-»
en
I-H
a>
>>
X
1—1
a;
>-
^
§"
1— t
u
>>
a,
^
0
■♦-»
CO
w
in mortality was reported, along with an increase in pupation time.
Little mortality was seen among the adults. Most adults recovered after
a period of inactivity.
Bees
Atkins et al. (1975) concluded that field applications of 1 kg /ha would
produce a dosage of 1.12 yg/bee and would be relatively non-toxic to
bees. Johansen (1959) reported that 2,4-D was non-toxic to bees
except when formulated as a alkanolamine salt or isopropyl ether.
Moffett and Morton (1975), Morton et al. (1972), and Moffet et al.
(1972), reported 2,4-D to be relatively non-toxic to bees (LDrn ~ ^'^^^
mg/1) except when diesel oil was used as a carrier (resulting in high
mortality). Moffett and Morton (1975) also reported that drownings
occurred when surfactants were added to drinking water.
Soil Organisms
Bauer (1961) noted that 2,4-D was very susceptible to breakdown by
soil microorganisms and that it showed no signs of impact on the soil
microbes at normal application rates. In a report by NRCC (1978), it
was concluded that at field concentration, phenoxy herbicides have no
dramatic effect on soil microbes. Magee and Colmer (1956) found that
the rate of oxygen absorption by three species of Azotobacter (a
nitrogen-fixing bacterium) was unaffected when they were exposed to
2000-5000 mg/kg 2,4-D amine. Teater et al. (1958) reported that
significant accumulations of nitrate occurred when 2,4-D amine was
added to incubated soil at 8.8 and 35 kg /ha, and that stimulation of
carbon dioxide evolution was significantly affected only at 35 kg /ha.
Gaur and Misra (1972) cultured seven species of the nitrogen-fixing
bacterium that grows symbiotically in legume root nodules, Rhizobium ,
in broth with 50-2000 mg/1 2,4-D. Growth of one of the species was
stimulated by 250 mg/1 and above; two of the species were slightly
suppressed by 250 mg/1 and above; and two other species were
significantly suppressed at 250 mg/1 and above. The effect on the
other two species in the study was not discussed.
11-84
Balasubramanian and Rangaswami (1973) concluded that the
concentration of bacteria, fungi, and actinomycetes populations
increased in number in the rhizospheres of sorghum sprayed with
2,4-D. Root exudations of sugars and amino acids also increased,
Dow Chemical U.S.A. (1972) investigated the effect that 2,4-D had on
earthworms. They found that no mortality was produced when worms
were immersed in 0.1, 1.0, 10.0, and 100 ppm of 2,4-D for 2 hours.
1000 ppm produced 100% mortality. They also found that there was no
effect on wireworms, springtails, mites, or other micro-arthropods at
typical field concentrations.
Bioaccumulation
Lowe (1964, cited by Rawls, 1971) found that the acid or ester of 2,4-D
disappeared rapidly from the tissues of fish and oysters when exposure
was discontinued. Studies by Erne (1966) concluded that 2,4-D amine
and alkali salts were not retained in tissues of pigs, chickens, or
calves, even following repeated administration. On the other hand,
Rodgers and Stalling (1977) and Shultz and Whitney (1974) showed that
fish accumulate residues that were unidentified metabolites of 2,4-D.
14
Stalling and Huckins (1975) found that C fragments were incorporated
into fatty acid, glycogen, and amino acid components of the fish.
In a report by NRCC (1978) it was concluded that 2,4-D was not
accumulated in major links in food webs, and that 2,4-D residues in
shellfish, benthic fauna, and fish reported by Smith and Isom (1967),
Whitney et al. (1974), and Coakley et al. (1964) were there as a result
of residues in plankton and plant pools. Residues in plants have been
observed to persist for 2 to 6 months by Wojtalik et al. (1971). Model
ecosystem studies by Isensee (1971) and Metcalf and Sanborn (1975)
suggest that at aquatic concentrations of 0.1-0.2 mg/1, 2,4-D
accumulation would be observed in algae and daphnids in magnitudes of
1 to 2 orders greater than in water.
11-85
Toxicity Data Evaluation
As summarized in the main body of this report, there is no clear evi-
dence available that indicates that 2,4-D is a carcinogen, although
considerable debate has been generated on the subject and further
study is needed. There is some evidence to suggest that 2,4-D causes
a weak teratogenic effect; however, the data present no firm basis for
conclusion. Although there are some conflicting results, most reliable
tests indicate that 2,4-D is not a mutagen. Insufficient information is
available on the toxicity of the various forms of dioxin found in 2,4-D.
The epidemological tests reviewed in this study are inadequate because
of small sample size and an inability to factor out the effects of other
chemicals to which the workers were exposed. Reports of neurotoxicity
are also suspect, due to an inability to factor out exposure to other
chemicals. Also, the neurotoxicity reported is difficult to make con-
sistent with the lack of neurotoxic effect from acute exposure in fre-
quent homeowner use for several decades.
No studies in EPA registration files have been conducted by IBT.
According to the Massachusetts Conservation Law Foundation, EPA
identified the following data gaps in registration files: acute toxicity,
tumor formation, reproduction, birth defects, neurotoxicity, and metab-
olism. Acute toxicity data have been submitted.
11-85. 1
F. DICAMBA
1. INTRODUCTION
Dicamba is the common name for the herbicide 2-methoxy-3,
6-dichlorobenzoic acid (Velsicol Chemical Corp., 1981) or
3,6-dicloro-o-anisic acid (TRW, 1981; Thomson, 1975), manufactured by
Velsicol Chemical Company. It is also known as Banvel , Banex ,
Dianat , Mediben , and Mondak (Thomson, 1976). Banvel 720 and
®
Banvel 520 are formulations that also contain 2,4-D (the DMA salt and
the isooctyl ester of 2,4-D, respectively). Dicamba formulations include
granules, pellets, an oil-soluble acid, and various water-soluble acids
and salts (Velsicol Chemical Corp., 1981). The structure of dicamba
is
0CH3
Other relevant physical and chemical characteristics are presented below
in the discussion of the fate of dicamba in soil and water.
2. TOXICITY
Acute Toxicity
Acute toxicity tests show a low order of toxicity for dicamba. Oral
LD_» values, summarized in Table 11-23, range from 1028 mg/kg to 2900
50
mg/kg for rats, and greater than 4640 mg/kg for mice. Guinea pig and
rabbits appear to be more sensitive with LD-- values of 566 mg/kg,
reported for both by Velsicol Chemical Corporation (1974a).
11-86
o
u
:i
o
O
o
a
u
o
u
w
>
o
U
e
O
'o
o
• rH
I— I
>
o
o
3
o
O
E
(1)
>
ISO
'55 o
> T3
o
U
•
s
u
o
.1-1
I— I
a;
>
03
C
•i-i
l-H
03
2
l-H
I
in
o
tn
e
o
H
O
U
cn
03
O
C
03
u
<
0)
(0
o
o
A
I
J
PQ
<
O
>^
H
I— t
U
X
o
H
<
O
w
H
O
<
00
O
(30
CO
E
o
C4
oJ
m
Q
3
O
in
r-
00
I
in
o
o^
o
<VJ
o^
o
+J
(NJ
ro
03
1
1
rt
r-
oo
o
(M
c^
o
o
o
o
o
00
+1
o
o
o
o
a«
1
o
00
CM
O
00
o
o
o
o
E
u
o
fa
<
Q
1 '^
OS n
oJ
o
H
>
03
CQ
oJ
<
Q
OS
£
o
m
u
(0
I d
nO 03
« I
fO O
03
<
<
<
Q
<
Q
03 o
u
•1-4
•-H
(0
I
o
u
o
* o
CO Oj
Although several methoxy derivatives of dicamba are less toxic than the
parent compound, 3,6-dichlorosalicylic acid, the major decomposition
product, is as toxic as the parent compound. Its oral LDj-n is 1440
mg/kg in rats (Zick and Castro, 1966),
Velsicol Chemical Corporation (1974a) found the dermal LD-- value to be
greater than 2000 mg/kg when technical Banvel and Banvel DMA salt (4
lb /gal) were administered to the skin of rabbits. In regard to inhala-
tion toxicity, they reported that the concentration of Banvel DMA in air
necessary to give a 50% probability of lethality in 4 hours was greater
than 200 mg/1.
In a study by Edson and Sanderson (1965), intraperitoneal adminis-
tration of technical grade dicamba to the rat resulted in an LD-- value
bU
of 80 mg/kg. When it was administered subcutaneously , the LD(.- was
1000 mg/kg.
TRW (1981) states that some formulations are extremely corrosive and
irritating to the eyes, citing a Velsicol Chemical Corporation Bulletin
(1974a). No other information was provided. A low-grade irritation of
the eye of the rabbit was noted when 0.1 ml of a 4 lb /gallon
concentrate of dicamba as the diethylamine salt (89.7%) was
administered. This disappeared rapidly and no injury to the cornea or
iris was observed (Velsicol Chemical Corporation, 1974b). When the
dimethylamine salt was applied to the eyes of the rabbits as a 0.2% or
2% aqueous solution in single or repeated doses for a week, no irritation
or injury was noted (Velsicol Chemical Corp., 1974b).
Subchronic Toxicity
Dicamba has a low order of toxicity in subchronic studies except at
high doses or long exposures. Dicamba as the amine salt was fed to
rats for 13 weeks at dietary concentrations of 100, 500, 800, and 1000
ppm. After 7 weeks there were no deaths, the pathology was negative,
and growth rates and food consumption were normal. After 13 weeks,
there still were no detectable effects at 100 or 500 ppm. However, at
11-88
800 ppm slight liver pathology was noted, and at 1000 ppm moderate
histopathological effects on the liver and kidney were observed (Velsicol
Chemical Corporation, 1974b). No significant toxic effects were ob-
served on rats fed for three weeks on diets containing 658 ppm to
23,500 ppm Banvel D, as reported by EPA (1975).
Edson and Sanderson (1965) conducted a feeding study using male
Wistar rats. For 15 weeks, the rats were fed diets containing 31.6,
100, 316, 1000, and 3162 ppm dicamba. At 1000 and 3162 ppm, they
noted a slight but statistically insignificant increase in the liver-to-body
weight ratio. They estimated that 316 ppm dicamba (equivalent to 19
mg/kg/day was the dose at which no adverse effect was seen.
Kudzina and Golovan (1972) concluded that there were no adverse signs
of toxicity in rats and rabbits fed 0.075 or 0.75 mg/kg/day for a period
of 6 months. The authors noted toxic effects in the animals fed 7.5
mg/kg/day, although these effects were unspecified.
A bulletin from Velsicol (1974a) stated that a mild irritation resulted
from administration of undiluted dicamba (dimethylamine Scilt) to the
skin of rabbits and rats for 2 weeks. No irritation was noted after the
dicamba was diluted 1:40 in water and applied to the skin for 30 days.
Mammalian Metabolism
Dicamba appears to be rapidly excreted from the body, as would be
expected as a consequence of its high water solubility. Rapid excretion
in urine was observed in a feeding study on dogs in which 88% of the
labeled dose was excreted unchanged and 12% was excreted in conjuga-
tion with glycine. (Velsicol, 1974a). When labeled dicamba was
administered orally to rats, 93%-99% of the label was excreted in the
urine as unchanged dicamba, with small amounts in the form of
glucuronide congugates. From 1% to 4.5% of the labeled material was
found in feces (Tye and Engel, 1967).
11-89
Oral administration of 20,000 ppm labeled dicamba to a heifer resulted in
the urinary excretion of unchanged dicamba, with a hydrolysis product
3 ,6-dichlorosalicylic acid also detected (Edson and Sanderson, 1965).
Only 73% of administered radioactivity was excreted after 7 days in the
urine of a Holstein cow fed 5 ppm dicamba for 4 days (St. John and
Lisk, 1969).
Special Studies
Carcinogenicity No evidence of tumor induction was observed in a dog
study in which purebred beagle dogs were fed dicamba at dietary levels
of 0, 5, 25, and 50 ppm for two years. In another study, no evidence
of carcinogenicity was seen when male and female Sprague-Dawley rats
were fed 0, 5, 50, 100, 250, and 500 ppm dicamba (USEPA, 1975). In
both of the above studies, no adverse effects were observed in
survival, food consumption, body weight, organ weight, hematology or
histology. Personal communication with Dr. David Whitacre (9/8/83) of
Velsicol Chemical Corporation indicates that the rat study was conducted
at least 15 years ago and that a new 2-year rat study, using an updat-
ed laboratory protocol, is nearing completion. Results will be available
in the late spring of 1984.
Teratogenicty / Reproduction A review by EPA (1975) cities two studies
which show no reproductive toxicity. In one study, Charles River-CD
rats were fed 206 ppm dicamba. No reproductive toxicity was observed
over a period of three generations. Similar results were found when
500 ppm dicamba was included in the diets of Sprague-Dawley rats
(USEPA, 1975).
Dunachie and Fletcher (1970) injected 10-400 ppm dicamba into chicken
eggs and found a 38% reduction in hatching at the highest dose. It
should be noted that there was a great deal of variability in the
percentage of hatching, and that no clear dose response was evident
for any of the 25 herbicides tested. Furthermore, the absence of a
physiologic maternal-fetal relationship during incubation makes this test
system highly questionable for assessing potential reproductive or
teratogenic hazards in humans.
11-90
k
Mutagenicity As summarized in Table 11-24, avcdlable studies show no
mutagenic effect. One of the studies showed mixed results (Anderson
et al., 1972). This study found that dicamba showed a statistically
significant (p = 0,05) increase in induction of rll mutants of the T.
bacteriophage. However, the herbicide did not result in a "marked
increase" as compaored to other substances, and no increase in mutations
was found in test systems using eight histidine-requiring mutants of
Salmonella typhimurium. Eisenbeis et al. (1981) tested dicamba alone
and dicamba in combination with atrazine. No increase in mutations
over controls was found in either test.
Other Information Related to Chronic Toxicity Bontoyan et al. (1979)
screened a variety of technical and commercial pesticide formulations for
the presence of nitrosamine contaminants. No such contaminants were
found in dicamba samples, although it should be noted that the level of
detection was only 1 ppm.
Summary An evaluation of important toxicity data is provided at the
end of this chapter.
3. MOBILITY AND PERSISTENCE
Fate in Soil
Dicamba has been found to be one of the most mobile of all herbicides
(TRW, 1981; USDA, 1973; Malina, 1973). In its pure form, dicamba has
a moderately low solubility (0.65 gm/100 ml at 25°C), but as the more
commonly used dimethylamine salt, it has a very high water- solubility of
72 g/100 ml at 25°C. Sodium and potassium salts are also highly water-
soluble (USDA, 1973). Friesan (1965) found that when an unspecified
amount of dicamba was applied to a sandy loam and eluted with 5 cm of
water, the herbicide reached a depth of 15 cm in 1 hour. Dicamba was
found to be the most mobile of 40 pesticides tested, with a mobility
value of 0.96 (the range for the 40 pesticides was 0 to 0.96) (Helling,
1971). In a study of 28 herbicides, dicamba was found to be more
mobile than all but one (2,3,6-trichlorobenzoic acid) (Harris, 1967).
After 63 weeks, dicamba had reached a depth of 68 cm in a sandy loam
(EPA, 1975; no primary source given). A review of the literature by
11-91
i
rsi
(—1
c-
00
o^
o^
■""^
^_^
^^
pH
f— 1
'~^
,,— V
CO
i-H
l-H
•
•
1— <
m
<»
l-H
CM
l-H
00
r-H
*J
■^
,_,
l-H
•
•
(U
a)
«J
•
n)
en
l-H
1—1
>*/
l-H
u
C
(U
C
0
w
4J
•»H
(U
u
0)
(U
(U
C
>>
^
>^
0)
0
r— i
0
0
o
o
• 1^
0
Pi
cu
Ph
<
W
2
cu
2
I
w
CQ
<
CQ
en
H
a:
H
>^
H
»-H
o
l-H
2
W
O
<
H
D
2
en
C
E
E
o
O
3
tn
(2i
00
ID
o
o
r-H
I
<
00
I
<
H
CO
u
(
CO
Q
■1-1
>
u
m
(U
£
^
-«-»
£
n
0
>>
Sh
en
rt
^
-M
o
CO
o
(U
03
H
cn
>^
nJ
W
tn
OJ
C
o
1-H
1 *
■♦^
rt
C
p-i
JD
rt
£
1— 1
l-H
0
<u
u
c
<u
0
;h
S
u
1^
■♦->
en
o
-~»
■•->
en
•<-l
D
o
u
•IH
u
u
CQ
Cx]
(
Velsicol (1981) states that many studies indicate that dicamba will move
vertically and that it has been shown to move with the flow of water
(no primary sources given except Naishtein et al., 1981). Dicamba can
also move up vertically into the root zone as evaporation draws soil
moisture upward (Harris, 1963).
The high mobility of dicamba indicates that dicamba does not adsorb
strongly to soil particles . Dicamba does not adsorb to illite clays
(Burnside and Lavy, 1966) . Kaolinite clays can adsorb some dicamba
because of their anionic exchange capacity (dicamba behaves as an
anion between pH 4.1 and pH 9.4) (Burnside and Lavy, 1966).
A number of studies have shown that dicamba is adsorbed on organic
matter (Grover, 1977; Khan, 1973; Stewart and Gaul, 1977). Corbin et
al. (1971) showed that dicamba is more strongly adsorbed at low pH.
Velsicol (1981) also states that the adsorption of dicamba is negatively
correlated with pH.
After summarizing both internal and publicly available studies, Velsicol
(1981) states, "In summary, dicamba is mobile in soil. High organic
matter or low pH may retard movement of the substance but certainly
does not eliminate it. Therefore, vertical soil mobility will account for
some portion of the loss of dicamba from surface soils."
The major soil degradation product, 3,6-dichlorosalicylic acid, is more
readily adsorbed than the parent compound, with at least 30% of the
applied material bound to soil colloids in a variety of soil types (Smith,
1974).
In regard to runoff, TRW (1981) concludes that this route of loss is not
likely to be significant because dicamba salts are so highly water-solu-
ble and quickly move downward in the soil. Runoff should result only
in cases where rainfall occurs very soon after application and is suffi-
ciently heavy to result in significant lateral as well as vertical move-
ment. Similar conclusions were reached by Velsicol (1981). Trichell,
et al. (1968) measured dicamba concentrations from two clay loam plots
11-93
(3% slope), one with sod and one that was fallow. After 24 hours, the
concentrations of dicamba in runoff water were 4.81 ppb and 1.60 ppb
from the sod and fallow plots, respectively. After 4 months, these
concentrations dropped to 0 and 0.018 ppb.
The persistence of dicamba is difficult to assess because of the over-
riding importance of the amount of water that moves through the soil.
Phytotoxic levels have been reported to persist from as little as 30 days
(Burnside and Lavy, 1966), to over 1 year (Dowler et sJ. , 1968).
Arthur D. Little, Inc., (1979) reviewed the literature to determine the
persistence of dicamba in sandy loam soil (a common soil in Massachu-
setts) cind found four studies indicating persistence ranging from 2
months to over a year. Velsicol (1981) states that dicamba will have a
half-life of less than 30 days under most conditions. Altom and
Stritzke (1973) showed that the dimethylamine salt of dicamba had a
half-life of 17-32 days when applied to forest and grassland soils at a
concentration of 2.47 ppm. A faster dissipation rate was observed by
Stewart and Gaul (1977), who applied an amine salt of dicamba to a
silty loam at rates up to 4.5 kg a.i./ha. After 42 days, 5% of the
dicamba remained. Audus (1964) and Cain (1966) found that within 10
months after application of up to 6 lbs/ acre of dicamba to an unspeci-
fied soil, all had disappeared below detection limits in the top 24 inches
of soil. Scifres and Allen (1973) state that at application rates of 1.12
kg /ha or less, dicamba should not persist longer than one growing
season when applied in spring.
In a laboratory study. Smith (1974) found that over 50% of dicamba in
moist, non-sterile heavy clay was lost in 4 weeks. The major degrada-
tion product, 3 , 6-dichlorosalicylic acid, increased as dicamba degraded,
but then decreased to non-detectable amounts in 9 weeks.
Numerous studies suggest that dicamba is stable to chemical hydrolysis
and that degradation is predominantly microbial (Smith, 1974). Smith
and Cullimore (1975) showed that while dicamba did not dissipate in
sterilized soils at 15°C, it did degrade significantly at the same tem-
perature in unsterilized soils.
11-94
I
The factors that affect microbial degradation of dicamba were reviewed
by Velsicol (1981). They found the most important factor to be a
healthy microbial population. The degradation of dicamba has been
shown to increase with conditions that promote microbial growth, namely
organic matter, moisture, and high temperatures (Arthur D. Little,
Inc., 1979). Addition of bacterial nutrient broth has been observed to
accelerate degradation (McClure, 1970).
A number of studies have also shown the pH of the soil to be an
important factor. In soils with a high percentage of organic matter,
the optimum pH for degradation of dicamba was found to be 5.3 (Corbin
and Upchurch, 1967). Velsicol (1981) states that dicamba was found to
be considerably more persistent at pH 7.5 than at lower pH's. Others
have found that degradation of dicamba increases with decreasing pH
(Swanson, 1969; Parker and Hodgeson, 1966).
Harger (1975) and Smith (1973, 1974) both state that during
degradation, dicamba is decarboxylated in the soil and the ring is
opened. The only degradation products documented by Smith (1974)
were 3,6-dichlorosalicylic acid and CO-. Velsicol (1981) states that in
addition to these two products, unspecified "tightly bound materials"
are produced.
Some loss of dicamba can be expected to occur from volatilization,
although the total amounts are probably not significant. After
incorporation of dicamba into soil, vapors were found to be toxic to
beans in a study by Centner (1964) (no time specified). In another
bioassay, volatilization of dicamba from corn leaves was detected for 3
days after the corn leaves had been treated (Behrens and Lueschen,
1979). These same authors, however, found very little loss of dicamba
during an 8-week period from autoclaved soils at 35°C and under
humidities ranging from 0% to 100%.
Residues and Persistence in Water
Residues of dicamba in streams have been found to be low. Bonneville
(1981, no primary source given) described a 3-year study in western
11-95
Washington in which 0.5 lb /acre of dicamba was applied by helicopter to
a transmission line right-of-way. In the first year, an (unplanned)
direct application was also made to the stream. In that year, 8 ppb , 1
ppb , and approximately 3 ppb were detected 30 hours, 48 hours, and 2
weeks, respectively, after application. In the second year, at an
application rate of 1 lb /acre, no dicamba residues were found. In the
last year, at the same application rate, dicamba residues peaked at 3
ppb after 4 hours and then diminished to non-detectable levels after 4
days.
For 14 months, Norris and Montgomery (1975) sampled the water from a
stream adjacent to a forest application of 1.12 kg/ha of dicamba. No
residues were detected beyond 11 days after application. Residual
levels peaked at 37 ppb in about 5.2 hrs, then declined to background
levels in 37.5 hrs.
Very little is known concerning the routes of loss in water.
Photodecomposition of dicamba is known to occur (USDA, 1973),
although the total amounts lost by this route are probably not
significant. There is some evidence to suggest that dicamba is removed
by adsorption to stream sediments (Norris and Montgomery, 1975) and
uptake by aquatic vegetation (USDA, 1973). Velsicol (1981) states that
dicamba has been directly applied to standing water and found to
dissipate rapidly (no data provided) .
Very little information is available on the degradation products of
dicamba in water. In the laboratory, Chirchirillo (1966) and Allen and
Scifres (1971) both report the formation of 3,6-dichlorosalicylic acid.
Yu et al. (1975) detected small amounts of 5 -hydroxy dicamba. Neither
metabolite was found in water in the field after forest spraying (Norris
and Montgomery, 1975) or after dry ditchbank treatment (Salman et al. ,
1972).
Indicators of Potential Ground Water Contamination
Table 11-25 provides information on parameters associated with the
mobility of dicamba. These parameters, and their associated
11-96
thresholds, have been suggested by EPA for use in assessing the
potential for pesticide contamination of ground water. A discussion of
these parameters and thresholds, and the methods for arriving at
designated values for individual herbicides , is presented in the main
body of the report as part of the discussion of the fate of herbicides in
the environment.
TABLE 11-25
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
DICAMBA
Indicator
Solubility
K
oc
Value for Dicamba
6500 ppm
(technical material)
at 20°C;720,000 ppm
(dimethyl salt)
Threshold
>30 ppm
Speciation at pH 5
Hydrolysis half-life
Photolysis hcdf-life
Vapor pressure
* ND = no data.
** Based and K,<1 (Velsicol) .
a
<150**
<300-500
Anionic
Anionic
(negatively charged)
ND*
>6 months
ND*
3.41 X
mm Hg
10'
at
-5
25^
>C
>3 days
<10~ mm Hg
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Information from the U.S. Forest Service (1974) and Velsicol Chemical
Corporation (1974a), summarized in Table 11-26, showed that dicamba
can be considered non-toxic to birds. LC_- values ranged from 673 to
50 °
2000 mg/kg for domestic hens, mallard ducks, bob white quail, and
pheasants.
11-97
(N]
I
<
en
Q
1—1
CQ
2
O
<
<
fa
o
H
U
ac
<«
rt
'J'
■^
p"-
c^
f— (
i-H
^
"^
^
•
•
0*
•
I-H
H
Jh
o
0
<u
u
^
U
"^
1— 1
u
,_
o
>
(^
'^
rt
'— '
Sh
u
o
(U
=
•fi4
K
•11
^
«k
W
S
s
=
0)
E
(U
(U
73
0)
■4->
■4-»
73
CO
OJ
-3
O
c
'o
0
C
0
fa
u
o
s-^
o
^-^
^
3
• l-H
s
• 1-H
•
CO
<
CO
I-H
<
w
0
a;
a*
0)
CI.
•
C/2
>
w
>
u
D
s
a
B
a
a
E
E
E
&0
^
CUD
tn
li
o
o
o
o
0-
a
W3
&0
dO
•4->
£
o
o
o
o
a.
a
E
r-H
o
o
o
o
E
E
o
•k
A
•k
•>
o
o
o
o
o
o
o
o
■^
■^
o
CO
o
o
1— (
rH
<—<
r— I
sO
v£)
o
r^
o
(NJ
A
A
A
A
^
•^
(M
sO
00
o
O
o
o
o
O
lTi
irt
ID
ir>
in
in
o
in
u
u
o
U
U
u
o
\n
O
J
J
J
J
J
J
o
J
>s
>^
>s
>^
>N
>>
J
•4->
p^
u
^
u
Sh
;^
^H
I-H
o
o
OJ
rt
(TJ
a
03
rt
03
03
03
in
in
V4
0
•4->
0)
0)
0)
0
o
U
• pH
•*-H
•f-H
• PH
•1-^
• <-(
J
J
0)
TS
^3
'0
TJ
-a
-0
0)
•»-»
+j
^
><
>»
>^
>^
>>
>>
3
u
rt
CO
OJ
rt
03
03
o
<
^3
1
1
1
1
1
1
<
1
00
1
00
1
00
1
00
1
00
1
00
CO
O
C/3
CO
CJ
T3
T3
03
I-H
la
2
CO
o
13
T3
03
I-H
I-H
OS
03
cr
xi
o
CO
o
3
T3
T3
}h
03
l-H
03
3
cr
•♦->
• IH
o
CQ
CO
o
3
73
!h
03
l-H
03
3
cr
•t->
•IH
o
03
CO
X
u
3
T3
CO
-t->
T3
03
u
CO
03
03
l-H
l-H
lU
03
J3
IS
Ph
0)
CO
<u
S
o
Q
o
fa
•
•f-4
•
03
00
l-H
CO
PH
a
"~-
1
0)
XI
'o)
>
effi
■"^
>
c
0
•^
C
03 '-^
oi
CQ .^*
•»
CQ
-^ *«*
(1^
X
0
1— (
'c3
.^OVO
(-H
1
»-H
0
C 00
(U
c
ech:
(86.
>
^
G
C 2
0
a
03 Q
<u
1 H
PQ
CQ
H
Fish
Table 11-27 shows that tests with rainbow trout, bluegills, spot, and
juvenile Coho salmon indicate that 96-hr LC-. values range from 23-130
ppm. A report by Arthur D. Little, Inc. (1979) considered dicamba
"moderately toxic" to fish, depending on the species. One study by
MiUs and Lowe (Gulfbreeze Lab, unpublished data [a]) reported a
48-hour LCj.- value for spot (Leiostomus xanthurus) of 1 ppm.
Lower Aquatic Organisms
Conflicting data are available on the effect of dicamba on lower aquatic
organisms. As shown in Table 11-28, studies by Velsicol Chemical
Corporation (1974a) and Sanders (1969, 1970) showed LC^.^ test results
of greater than 100 ppm for a variety of aquatic crustaceans.
However, studies by Sanders (1969) and the U.S. Department of the
Interior, FWPCA (1968) reported toxicity levels for a marine amphipod
(Gammarus lacustris) of between 5.8 and 10.0 ppm. Mills and Lowe
(Gulbreeze Laboratory, unpublished data [a]) reported an ECj.. (for
48-hour exposure) as 1.0 ppm. The same study showed oysters to
have a 50% reduction in shell growth after exposure to 5 ppm for 96
hours .
Livestock
Malina (1973) reports that dairy cattle given food with residues from 10
to 400 ppm of dicamba showed no adverse reactions. Assays of the milk
showed no residues at the lower levels, and residues not exceeding 0.15
ppm appeared in the milk after the cow was fed 400 ppm for 9 days.
Vital organ samples showed no trace of dicamba when cattle grazed for
30 days on pasture treated with 5 and 10 lb Banvel/acre.
Bees
Available studies present conflicting results in regard to the toxicity of
dicamba to bees. A study by Atkins et al. (1973) reported that expo-
sures of 90.65 yg/bee produced a mortality of 2.58% after exposure for
96 hours. Edson and Sanderson (1965) reported an LD-_ of 3.6 yg/bee
when administered orally in a 20% solution.
11-99
<0
u
u
3
o
a
u
o
U
u
E
0)
U
^•*
o
u
>
'S'
c^
(T-
rH
(U
u
•^
>
u
«— s
di
1—1
in
r-
o^
•4J
(— (
cn
s.^
(U
»H
0)
0
Ci4
c
w
cu 3
4)
J3
(U
<u
fTt
}h
•«->
«s
3
-0
0)
*^
X,
(U
(0
o
P-4
J
3
a
-a
c
c
3
rt
«K
cn
CO
SI
•^
cd
2 J
E
W
t— t
Ci*
2
O
<
C£i
2
1
<
U
HH
w
Q
J
CQ
|JL4
<
O
H
H
U
U
u^
b
u
w
E
H
(0
(0
Cfl
H
CO
(U
u
(U
CM
f^
1— 1
•"«»
&0
"~~.
""^
bfi
E
bO
bO
s
E
a
o
o
o
ir^
Lr>
00
o
m
cn
rH
1—1
o o o
in in m
u o o
J J J
V« V4 Sh
42 j: j:
I I I
sO O sO
O^ O^ CT^
cn
3
cn
3
O
V4
o
c
o
o
U
J
I
a
a
a
£
a
a
a
a
a
E
a
a
E
a
a
a
a
a
a
a
cOinLnoococnirtrj
I— I m cn rvj I— I
fva
a
o o- o o o o o o
mLomtnLniriLnvn
OUUOOOJJ
JJJJJJHH
I
QO CO
u
^ h ^ Vl
X X X X
I I I I
^ sO ^ vO
(M (js (M O^
U U
I I
^ 00
c
^
J3
c
CO
CO
•t^
•<-«
«f-i
a
^-4
MH
c
c
73
3
3
«J
CO
CO
(U
>— <
_^
^
.!-<
1— 1
a
00
&1
a;
(U
(U
(U
3
3
,£:
t-^
i-H
w
CQ
CQ
3
O
3
O
3
o
u
5
o
c
o
c
bo 00
„ _ _ (U D
^ ^'^•'^•'^3 3
p-4 1-4 nl (0 n) 1-^ I— I
O
c
o
£
CO
o
o
o
CO
o
o
u
I
a
a
o o
irt to
O U
^4
I
00
CO
3
a
o
CO
o
•l4
J
Oci Pi Cri CQ CQ U U
CO
3
3
U O CO
a
o
<
S
Q
•♦J
■3
"rt
'id
CO
g
&0
<
(«
^
:s
P3
s
Q
i-H
Tj»
(tf
•k
u
ik
a
c
13
>
c
X
a
M
<o
CTJ
H
CQ
Q
(0
•r4
a
m
I— t
>^
X
a
a
o
4
TABLE 11-28
EFFECTS OF DICAMBA ON LOWER AQUATIC ORGANISMS
Species
Daphnia
Grass shrimp
Fiddler crab
Sowbug
Crayfish
Seed shrimp
Brown shrimp
Test'
48-hr LC
96-hr LC
96-hr LC
50
50
50
48-hr TL
50
48-hr TL
48-hr TL
48-hr LC
Gammarus lacustris 24-hr LC
48-hr LC
Cypridosis vidua
Palaemonetes
kakiakensis
Orconectes nais
Crassostrea
virginica
96-hr LC
48-hr LC
50
50
50
50
50
50
50
48-hr LC
48-hr LC
96-hr LC
50
50
50
Result
111 mg/1
>100 mg/1
>180 mg/1
>100 ppm
>100 ppm
>100 ppm
1 ppm
10 ppm
5.8 ppm
3.9 ppm
>100 ppm
>100 ppm
>100 ppm
5.0 ppm
Source
Velsicol Chemical Corp. (1974a)
Sanders (1970)
Mills and Lowe (Gulfbreeze
Labs, unpublished data)
Sanders (1969)
USDI FWPCA (1968)
Sanders (1969)
Sanders (1970)
Mills and Lowe (Gulfbreeze
Labs, unpublished data [b])
Asellus brevicandus 48-hr LCj.^ >100 ppm Sanders (1970)
Technical Banvel used in all studies.
11-101
other studies by Morton et al. (1972) and Atkins et al. (1975), in f
which bees were fed or dusted with dicamba at suggested field concen-
trations, produced no significant mortality.
Soil Microorganisms
User handbook information supplied by the manufacturer stated that soil
microorganisms were not harmed by dicamba (Thomson, 1975). Cain
(1966) and Andus (1964) noted that Bacillus cereus var. mycoides was
capable of decarboxylating dicamba.
Bioaccumulation
Dicamba is readily soluble in water, and a report by TRW (1981) con-
cluded that there was no evidence to suggest that it was magnified in
the food chain. No data were provided.
Toxicity Data Evaluation
Data on the carcinogenic, mutagenic, and teratogenic effects of dicamba
are inadequate to enable conclusions to be drawn. Additional data need i
to be generated in regard to all these effects. (Although, according to
the registration standard, one teratogenicity study using female rabbits
has been reviewed and found to show no positive effects.)
A number of studies on dicamba were conducted by IBT. Of the muta-
genicity tests, two using mice were found to be invalid, and no
response has yet been made by Velsicol regarding their replacement.
One mutagenicity test using bacteria was also found to be invalid.
Velsicol has notified EPA that it does not intend to replace that test.
One study in EPA files on the mutagenicity of dicamba was not con-
ducted by IBT.
A teratogenicity and reproduction study done by IBT were also found
to be invalid. The former has been replaced, and the latter has been
determined to be not required by EPA. Several teratogenicity and
reproduction studies conducted by other laboratories already exist in
EPA files. Finally, a chronic /carcinogenicity study is currently being d
replaced by Velsicol. ^
11-102
In its registration standard review, EPA decided the following infor-
mation is required to be submitted before products containing dicamba
can be reregistered: 90-day feeding study on nonrodents; 21-day
dermal study; 90-day inhalation study; chronic oral study on 2 species;
oncogenicity on 2 species; gene mutation; chromosomsd aberration; and
other mechanisms of mutation.
11-102. 1
G. DIQUAT
1. INTRODUCTION
Diquat is the common name for the herbicide 6,7-dihydrodipyridol
pyrazidinium dibromide, produced by Chevron Chemical Company. It is
® ® ®
also known as diquat dibromide, Reglone , Aquacide , Dextrone , and
Weedrite®. (Thomson, 1975; Ouellette and King, 1977). Diquat is a
quaternary salt of 4,4-dipyridyl, with the following chemical structure:
2+
2Br-
Relevant chemical and physical properties are presented below in the
discussion of the fate of diquat in soil and water.
2. TOXICITY
Acute Toxicity
Toxicological information indicates that diquat can be considered
moderately toxic. Thomson (1975) reports an ^^cn of 231 mg/kg (no
test organism given). Manzo (1979) reports an LDrn for rats to be
400-440 mg/kg. A Material Information Bulletin by Chevron Chemical
Company (1982) states that diquat may be toxic to humans if swallowed,
and that the oral LDcn ^°^ rats is 600 mg/kg for females and 810 mg/kg
for males. Calderbank (1968) reports oral LD^^ values ranging from 30
to 400 mg/kg for cattle, mice, dogs, rats, and chickens. Cattle were
the most sensitive and chickens were the least sensitive.
11-103
In regard to dermal toxicity, the Material Information Bulletin by
Chevron Chemical Company (1982) states that the acute dermal LDj.^ for
rabbits is 260 mg/kg (male) and 315 mg/kg (female).
Both the label and the Material Information Bulletin by Chevron
Chemical Company (1982) state that contact with the skin may cause
severe irritation to skin, and that diquat may be fatal if absorbed
through skin. No data is cited. These two information sources also
state that diquat may be fatal if inhaled. The Material Information
Bulletin also lists an acute inhalation LC^/> for rats (exposed for 1
hour) to be less than 6.1 mg/1, and that "breathing spray mist may
cause nasal, throat, and respiratory tract irritations."
Subacute /Sub chronic Toxicity
Black et al. (1966) and Calderbank (1968) report no observable adverse
effects on several animals tested by feeding silage and hay containing
up to 20 mg/kg diquat for 90 days. Howe and Wright (1965) noted no
toxic symptoms for sheep and calves given drinking water treated with
20 mg/1 diquat for 30 days.
Mammalian Metabolism
14
Stevens and Walley (1966) fed C-diquat (5 to 20 mg/kg) in single oral
doses to lactating cattle and found radioactivity largely as metabolites in
urine (2.6%), in milk (0.02%), and the remainder in feces. Daniel and
Gage (1966) and Black et al. (1966) demonstrated that metabolites in
rats and sheep originated from microbial breakdown in the gut.
Work by Stevens and Walley (1966), Black et al. (1966), Calderbank
(1968), and Litchfield et al. (1973) suggests that the milk and meat of
animals injesting "normal" levels of diquat would be free of
contamination due to the rapid excretion from the body (largely as
metabolites). Daniel and Gage (1966) report that diquat is a highly
soluble divalent cation that is stable and not metabolized to any
significant extent after administration to animals.
11-104
Special Studies
Carcinogenicity No data were located regarding the carcinogenic poten-
tial of diquat.
Teratogenicity / Reproduction Limited data suggest a possible teratogenic
effect. CFLP mice were given either repeated administrations (4) of a
low dose (2,7 mg/kg) or a single administration of a higher dose (11.0
mg/kg). The repeated administration of the lower dose resulted in a
retardation in weight gain. At both doses* changes in the skull,
vertebrae, sternum, and limbs were observed. The number of dead or
resorbed embryos was increased 9% with the single administration of the
higher dose, and 11% with repeated administration of the lower dose.
Using the egg injection technique, Dunachie and Fletcher (1970) noted
an embryotoxic effect after administration of 10 ppm. Hatching was
reduced 93%, compared to controls. It should be noted that a great
deal of variability in the percentage of hatching was seen and no clear
dose response was evident for any of the tested herbicides. Further-
more, the absence of physiologic maternal-fetal relationships during
incubation make this test system of questionable value in assessing
potential teratogenic hazard to humans.
Mutagenicity As shown in Table 11-29, available studies indicate that
diquat is not a mutagen.
Summary An evaluation of important toxicity data is provided at the
end of this chapter.
11-105
o
a-
o^
00
r~-
r^
o^
^.^
a^
c^
1— 1
^
(—1
I— 1
^"^
"^^
^^
•
1— 1
•
1— t
<«-N
•
13
*~^
nj
rt
•»-»
•
•<-> =
a^
-^-t
(U
1— I
(U
(—1
(U
(fl
(0
•f-i
•iH
(U
(U
•4->
(U
C
bO
c
u
CL
00
•r4
GO
13
>>
•I-l
CO
U
^
o
0)
rt
0)
n>
<u
w
w
d^
CQ
b
pa
n
C
o
CO
CO
2
XI
C
E
m
oo
■i-i
o
)30
c
n
I
CQ
<
<
a
m
H
m
w
H
>H
H
(—1
u
o
<
D
2
CO
(U
E
S
o
O
3
CO
'^H CO CO
o C .
•
rally
ontai
or 7
•1-1
■♦->
uo
3.
b "^ .
,i*J
° HD _ ^ —
■■~~
bO
CO
<u
1— (
o
E
c
3-
O
o
1
° |o ^
o
o
o
o pc; ra E
r^
•^
*
T
0)
•4-*
c4
O
o
o
rt
in
«
•«->
(«
C
te
plani
mogei
0)
1— H
a
cti , 0
~««
r— 1 >H /H
bO
;3.
3. 0) c
o
1— 1
> >>
1
c^ ;5 N
r— 1
c
•
O +1 (I)
o
II
II
H
I
II
n
ll
•I
•I
v
vO
o
t-H I,
o
u
u
E
o
0)
E
CO
3
(U
o
■♦->
CO
E
5>>
C/3
o
>
■4->
CO
•i-i
>
.1-1
■M
0)
a
E
o
X)
a;
CO
o
2
CO
1—1
CO
I— t
1— H
• I-I
bOl
(^
CO
O
1—1
o
o
•I-I
1—1
(U
o
u
(0
(U
CJ
H
S
o
■»->
CM
0)
rt
•1-1
CO
•IH
>
u
(U
u
CO
o
E
o
u
o
CJ
o
■I-I
CO
u
>
C
o
u
0)
(30
CO
0)
CJ
CO
(U
u
;h
E
CO
(U
o
H
E
o
CJ
o
I/)
l-H
I— I
(U
C
O
£
l-H
CO
CO
E
<
CO
E
<
X)
;h
^
O
to
">>
l-H
1—1
• I-I
en
o
o
<VJ
r-
^-N
x-^
o^
CO
1— 1
1—1
oo
00
cr>
<T>
«i n)
d) Oi
•i-i
o
2
en
•§
a.
(ti
C
o
en
(U
<
r-
c^
o^
l-H
u
^^
(U
^— «.
cr-
y-^
X
o
r-
f— 1
'4->
00
a-
00
3
o^
rH
o^
1— (
N^,/
r— 1
O
•
•
•
TJ
1-H
l-H
c
rt
«J
■M
rt
••->
<u
4->
•I-I
•1-t
0)
■4-»
E
0)
^
&0
m
4:
o
.|H
^
r— 1
o
c
o
^
0
(U
u
0
Pi
CQ
eu
cu
^
H
<
-'-N
D
Q
a
(i3
(—1
D
Q
2
1— 1
••
H
W
2
H
0
w
0
w
H
>H
1
H
H-l
t—i
H-1
0
CQ
<
I— 1
2
W
<
D
S
E
E
o
U
:3
CO
0)
01
l-H
o
S
c
•1-1
'0
0
E
rt
• rH
(0
^
>>
0
w
$H
0)
•4-»
^
(0
u
(U
en
H
W
o
0)
•4->
OJ
l-H
a
~«»
bo
E
3.
■'''^.
0
00
0
3.
0
l-H
0
1
0
0
vn
(M
(0
0)
(n
r-H
■♦-»
1 — 1
0
'St*
H
c
CO
<
2
tn
<u
■<->
>>
u
0
0
0
1—1
a
0
-4-*
l-H
C
0
^ (U
Q
pC
^4
J>^
N
ants 0]
iophag
di
(U
u
I-H
E
l-H
0
•4-»
E
■IH
^3
c
C
0
ti ^
0)
rt
nJ
00
3 (U
S1^
0
E
3
E
;3
r~4
HH «»
en
E
3:
PCj
(U
K ^
pL.
^
P
n
•3
u
■4-»
n)
u
•iH
Td
C3
CO
0)
en
•♦->
a
3. MOBILITY AND PERSISTENCE
Fate in Soil
Limited information is available on the fate of diquat in soil and water.
Most of the information presented below comes from a review by
Simsiman et al. (1976), who presented little detail regarding the re-
viewed studies.
Given these qualifications, however, it appears that diquat has low
mobility, since it is adsorbed strongly by clay and organic matter in
the soil. The bypyridyl herbicides (including diquat) were retained in
the upper 0.01 cm of soil after elution with water equivalent to 11
months of natural rainfall, even in sandy soil (Coats et al. , 1966). It
has been estimated that about 10,000 kg /ha of diquat would be needed
to saturate the capacity of a sandy clay loam soil to adsorb diquat
(Knight and Tolimson, 1967).
Diquat is very strongly adsorbed to clay particles and can occupy the
entire cation exchange capacity of montmorillonite and kaolinite, and
from 30%-90% of the capacity of vermiculite (Weber et al. , 1965; Weber
and Weed, 1968; Weed and Weber, 1969; Dixon et al., 1970).
Adsorption onto clay appears to be independent of pH and temperature,
and equilibirium ( adsorption /desorption) is reached after an hour
(Harris and Warren, 1964; Weber et al. , 1965; Coats et al. , 1966).
The amount of montmorillonite in the soil is particularly important in
determining both persistence and mobility. Because diquat molecules
can occupy the spaces between the layers of montmorillonite, diquat is
strongly retained once it is adsorbed. Only 5%-10% of the bound diquat
can be released from montmorillonite by competing cations (Al , Ba ,
Ca , Mg ) , while 80%-90% can be released from kaolinite and
vermiculite (Weber et al. , 1965; Weber and Weed, 1968; Weed and
Weber, 1969). Diquat can be desorbed from montmorillonite, however,
by similar organic cations, such as paraquat. Paraquat displaces
50%-90% of the bound diquat on montmorillonite and 100% on kaolinite
(Weber et al. , 1965; Weber and Weed, 1968).
11-108
Diquat is also readily adsorbed onto organic matter such as humic
substances (Damanakis et al., 1979), organo-clay complexes (Khan,
1973), and peat, muck, and organic soils (Harris and Warren, 1964;
Scott and Weber, 1967; Tucker et al. , 1967). Binding to organic
matter appears to be weaker than binding to clay, Diquat was
displaced more readily from organic matter than from clay when exposed
to solutions of competing inorganic cations (Simsiman, et al. 1976).
Although no data is presented, Simsiman et al, (1976) suggests that
diquat may move by erosion and runoff because of its tendency to
accumulate in the upper layer of soil.
Microbial degradation of diquat has been demonstrated by a number of
investigators (Baldwin et al. , 1966; Tu, 1966; Slodki and Wickerham,
! 1966; and others). No degradation of diquat occurred under sterile
I conditions in a study by Weber and Coble (1968) using labeled diquat
' and soil in nutrient solution cultures. Under unsterile conditions,
, decomposition of diquat released labeled CO_. The metabolic pathway of
t diquat has yet to be determined (Simsiman, et al. 1976).
I
! It should be noted that diquat adsorbed to montmorillonite is not
available for microbial attack (Weber and Coble, 1968). Montmorillonite
may thereby increase the persistence of diquat. Unfortunately, no
information regarding the half-lives of diquat in various soils is
available.
Photode gradation may be an important route of loss of diquat on the
surface of soils and on plant surfaces. Ultraviolet light has been found
to degrade diquat rapidly (Slade, 1965 and 1966; Coats et al., 1966;
Funderbank et al. , 1966; Slade and Smith, 1967).
Simsiman et al. (1976) summarizes a review of the information on the
fate of diquat in the soil with the following statement: "The avenues of
loss of diquat in soils seem to be through photochemical and microbial
degradation. Since adsorption tends to slow the rate of these
11-109
processes, it is likely that diquat will accumulate in soils, particularly
those containing montmorillonite . "
Persistence in Water
Diquat has been observed to disappear rapidly from natural waters
(Coats et al. , 1964; Grzenda et al. , 1966; Frank and Comes, 1967; Yeo,
1967; Hiltibrand et al. , 1972). Diquat residues were found to be
undetectable after 8 days in a study by Coats et al. (1964), and after
4 days in a study by Frank and Comes (1967). Yeo (1967) found only
"trace residues after 12 days when diquat had been applied at the rate
of 0.125 to 2.5 ug/ml.
It appears that diquat dissipates by adsorption to sediments and
suspended particulate matter and uptake by aquatic plants (Davies,
1964; Grzenda et al. , 1966; Frank and Comes, 1967; Yeo, 1967;
Hiltibrand et al. , 1972; Simsiman and Chesters, 1975). Absorption of
diquat by aquatic plants may be a significant route of loss, as
suggested by the ability of aquatic plants to concentrate the herbicide
by a factor of 50 after 4 days from an initial concentration of 0.5 yg/1
(Newman and Way, 1966). In another study, an initial concentration of
0.62 yg/1 disappeared from pond water in four days, but was then
detected after 24 days in sediments, increasing in the sediments to a
concentration of 37 yg/g after 56 days. (Frank and Comes, 1967).
Simsiman et al. (1976) suggests that a significant portion of the herbi-
cide is absorbed by the weeds, and that decomposition of those weeds
is necessary before the diquat becomes concentrated in the sediments.
After being adsorbed by the sediment, it appears that diquat persists
for a considerable time. Four years after 0.3 kg /ha was applied to
water bodies, concentrations of diquat up to 1.7 yg/g were found in the
sediment (Beasley, 1966).
11-110
Indicators of Potential Ground Water Contamination
Table 11-30 provides information on parameters associated with the
mobility of diquat. These parameters, and their associated thresholds,
have been suggested by EPA for use in assessing the potential for
pesticide contamination of ground water. A discussion of these
parameters and thresholds, and the methods for arriving at designated
values for individual herbicides, is presented in the main body of the
report as part of the discussion of the fate of herbicides in the
environment .
TABLE 11-30
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
DIQUAT
Indicator
Solubility
K
oc
Speciation at pH 5
Hydrolysis half -life
Photolysis half-life
Vapor pressure
Value for Diquat
700,000 ppm at 20°C
ND*
Cationic
(positively charged)
ND*
ND*
Non-volatile
Threshold
>30 ppm
<300-500
Anionic
(negatively charged)
>6 months
>3 days
-2
<10 mm Hg
* ND = no data.
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
The limited data available suggest that diquat is not toxic to test birds.
Heath et al. (1972) and Hill et al. (1975) report LC-^ values that range
from 1346 to >5000 ppm for bobwhite quail, Japanese quail, pheasants,
and mallard ducks. Tucker and Crabtree (1970) report the LDcn ^°^
mallards to be 564 mg/kg.
11-111
Fish
The data shown in Table 11-31 indicate that diquat is somewhat toxic to
a number of species of fish. The 48-hr TLj._ values range from 11.7
mg/1 for lake emerald shiners to 220 mg/1 for fathead minnows.
Because diquat is frequently used for aquatic weed control, a number
of studies have been done on the effect on fish under field conditions.
Gilderhus (1967) found that when diquat was added at a rate of 0.5 to
4.0 mg/1, there was some mortality of mosquito fish; other fish were not
harmed by these concentrations. The same study showed that no
mortality occurred among fingerlings and adult bluegills exposed to 1
and 3 mg/1 in artificial ponds. Blackburn and Weldon (1963) observed
no toxicity to fish over a 3-year test using diquat as an aquatic
herbicide in concentrations of 2.5 mg/1 or less. However, Hiltibran
(1967) reports that bluegill fry, lake chubsucker, and small-mouth bass
died within 1 to 4 days of exposure to 1.3 to 2.5 mg/1 of diquat.
Lower Aquatic Organisms
Table 11-32 summarizes available data, most of which resulted from a
study by Wilson and Bond (1969). This study concluded that amphi-
pods were very sensitive to diquat, while other invertebrates were able
to tolerate higher levels.
Livestock
Cattle may be somewhat sensitive to diquat. Calderbank (1968) states
that the LD_- value for cattle is 30 mg/kg. Thomson (1976) states that
diquat should not be used in the drinking water of animals. On the
other hand, Black et al. (1966) and Calderbank (1968) found no
adverse effects and no detectable residues in milk or tissue. Also,
Howe and Wright (1965) observed no toxic symptoms when sheep and
calves were fed water with 20 mg/1 of diquat for 30 days.
Bioaccumulation
Gilderhus (1967) and Calderbank (1968) found that the accumulation of
diquat in the tissues and organs of fish is negligible except in the
digestive tract. Hiltibran et al. (1972) and Beasley (1966) suggest that
11-112
u
u
o
U)
^^^
c
o
'C
nO
V
o^
^
i-H
^-^
c^
y
■^^
r-
o
•iH
nO
o^
cu
•
1— (
r— 1
vO
-d
'^^
(0
vD
c
•
0) =
:3
1— 1
o
^
a;
73
S
(U
(U
J3
a
X
TJ
a
u
o
o
1— t
-r-l
0
3
CQ
CQ
O
u
w
CO
>£)
O^
I-H
>-^
^
c
u
^ii^
^^
y-^
^-^
r-
o^
r^
cr-
nO
nO
>c
vO
CT^
<T-
o^
1— 1
T3
C
II
1966)
1— 1
I-H
1—1
c
s
P
(U
3
$H
>^
^^^
Jfl
I-H
^
0
0)
)h
Vi
^
0)
-0
0)
-0
%
^
o
I-H
•l-l
1— t
•IH
^
W
U
o
<
o
{
I
CQ
<
I-H
1X4
O
H
H
<
a
o
H
o
HH
X
o
CO
E
CO
0)
(0
ID
H
in m Lr>
•
•
•
un
o^
00
00
CO
(M
CM
Cs]
/T. O O
^ rH rH
•"^ •^ <NS
o
o
o
O
"!»<
o
CM
CO
I-H
rsi
(N3
I-H
o
(N3
00
•
I-H
vO
A
00
o
o
0
00
■4->
•«->
ir>
in
fM
o
o
vO
in
rg
(
ooooooooooooooooooooo
ininLnLfiLnLrtinininininmininLnininminmif)
u
1
u
1
u
1
u
1
u
1
u
X>
1
u
X>
1
u
X.
1
u
1
u
1
u
1
u
1
u
1
1
u
1
u
1
1
u
1
u
1
u
1
u
1
1
1
00
I
oo
1
1
00
1
1
00
1
0^
1
Csl
1
00-
1
1
1
fM
1
00
1
0^
1
00
1
1
00
1
0^
1
0^
1
in
o
a
I-H
CO
M
O
o
c
o
s
00
:3
U
W PQ
(0
o
no
0)
u
0)
C
•IH
X
(0
rn
'O
(0
I-H
u
<u
<0
S
cu
0)
•c
M
H->
rt
m
hJ
3
o
V4
o
•13
v
M
•IH
a
rd
CO
(0
• iH
>>
I-H
•*->
T3
u
I-H
I-H
0
0
(d
2
0
^
0)
u
o
M-l
vO
sO
^—N
o^
/-^
o^
1— 1
o^
sO
>— '
vO
CT*
a^
pH
i-H
TJ
o
^3
C
:3
C
0
H
O
CQ
73
CQ
73
C
'd
C =
= OJ
ti!
ni
>^
(tf
fi
^
fi
O
(0
0
CO
0
(n
1— 1
^
1— 1
.rH
•IH
^
O
^
o
(0
C
8
u
o
CM
CO
I
•J
PQ
<
en
H
<
EQ
H
>
l-H
u
H
<
a
<
o
H
H
<
a
E
;3
(0
0)
00
in
o
-^
o
o
o
O
o
o
O
o
r-
•
o
in
CO
o
o
o
o
o
o
rH
m
sO
1— 1
>J3
CO
rH
i-i
I-H
1— 1
r-\
rH
o
I-H
A
I-H
I— t
I
o
H
I-H
u
I-H
X
o
(0
H
o
o
o
O
in
O
hH
O
o
o
0
0
0
0
0
0
0
0
0
0
0
in
in
in
in
in
in
in
in
in
in
in
in
in
in
in
in
in
J
J
J
J
J
J
J
J
J
J
H
J
hJ
J
J
J
J
H
H
H
H
H
H
H
H
H
H
J
H
H
H
H
H
H
h
^
u
Vh
^
h
h
Vh
$^
u
^H
V^
;h
u
^
^
u
u
1
t
1
1
1
rd
4:
1
1
1
1
43
1
1
1
1
1
1
1
1
1
1
oo
1
1
1
OO
1
1
1
00
1
1
->*
1
00
1
vO
1
1
00
1
1
00
1
00
C\J
■^
O^
(M
CO
•>ii<
a^
(VI
•^
a^
<N3
^
0^
CM
■^
a^
rr
-^
Ui
(U
•I-l
u
(U
a
CO
Xi
c
a,
"» >>
a
'0
^
'0
•^4
>.j::
•s
0
a
• I-H
S
«J
HH
-s
^ c
J3
•i-t
c
Si
>>
en
• l-H
^3
0)
msel
rago
E
(0
T3
<tJ
rt
rt
c
rt Q
<
Q
2
U
^
Q
U
CO
diquat is excreted readily from fish and that residues disappear when
the fish are transferred to water containing no diquat.
Toxicity Data Evaluation
Insufficient information is available to assess carcinogenic or teratogenic
effects of diquat. Mutagenic data are sufficient to strongly suggest
that diquat is not a mutagen. The minority of positive mutagenic
results are from less-reliable tests.
Several studies on diquat were conducted by IBT. A chronic oral test
and two studies on reproductive effects have been replaced by Chev-
ron. (Several chronic oral studies and one reproductive study con-
ducted by other laboratories already existed in EPA files.) Regarding
two reproduction /residue studies done by IBT, one has been determined
to be valid; the other is under EPA review.
EPA is currently identifying data gaps in their registration files.
11-115
H. DIURON
1. INTRODUCTION
Diuron is the common name for the herbicide 3-(3,4-dichloro-
phenyl)-l,l-dimethyl urea (Thomson, 1975) manufactured by Du Pont.
It is available commercicdly in formulations known as dichlorfenidim,
DCMV, Di-on , Diurex-Di-on , DMJ , Karraex , Marmex , and
®
Sup'r-flow (Thomson, 1975), or as Krovar , a mixture of diuron and
bromacil (Ouellette and King, 1977). Diuron has the chemical structure
Diuron is a white solid that is non-corrosive and non-volatile, having a
-5
vapor pressure of 0.31 x 10 mm Hg at 50°C (Ouellette and King,
1977). Other chemical and physical properties are presented below in
the discussion of the fate of diuron in soil and water.
2. TOXICITY
Acute Toxicity
Available information suggests a low order of toxicity for diuron. The
LD for technical diuron is 3400 mg/kg (Hodge et al. , 1967). The
®
LD-^ for Karmex (80% diuron) is 6964 mg/kg for male rats and 3956
(S)
mg/kg for female rats (Du Pont, 1983a). Application of Karmex to
abraded skin of rabbits indicated a dermal LD-. of >2000 mg/kg. No
irritation or mild irritation occurred when technical diuron was applied
to intact or abraded skin of guinea pigs. No irritation was seen when
technical diuron (as a 50% aqueous paste) or Karmex (0.05 g aqueous
11-116
paste) was applied to intact human skin (Du Pont, 1983a). A mild
hyperkeratosis was reported by Hill et al. (1981) when diuron was
applied to rabbit skin at doses of 4.3 mg/ml/day and 3.4 mg/ml/day.
A very mild transient conjunctival irritation was produced by
administration of 10 mg of powder or 0.1 ml of a 10% suspension of
®
Karmex to rabbit eyes (Du Pont, 1983).
Subacute / Sub chronic Toxicity
Growth depression and increased erythropoiesis was noted in rats after
dietary administration of ten daily doses of 1000 mg/kg diuron (Hodge
et al. , 1967). No growth depression occurred at 400 ppm in a 90-day
feeding study with rats. Growth depression was slight at 2000 ppm and
marked at 2500 ppm. In the same study, slight anemia was noted in
females at 250 ppm, and at 2500 ppm in both sexes. At 2000 ppm and
higher, an abnormal blood pigment was observed (Hodge et al. , 1967).
Mammalian Metabolism
No tissue storage occurred in either rats or dogs after they were fed
25-2500 ppm diuron for 9 to 24 months. Excretion in both urine and
feces was noted and included N-(3,4-dichlorophenyl) urea as well as
small amounts of N-(3,4-dichlorophenyl)^N'-methylurea, 3 , 4-dichloro-
aniline, 3,4-dichlorophenol, and unchanged diuron.
Special Studies
Carcinogenicity Limited data suggests that diuron is not carcinogenic.
Innes et al. (1969) administered 464 mg/kg diuron by gavage to mice on
days 7-28 age, followed by the addition of 1400 ppm in the diet for
approximately 18 months. No increase in the incidence of tumors above
control values was seen. In a review of available data (including
registration material), EPA (1981b) stated that no indication of car-
cinogenicity was observed in a 2-year feeding study with dogs and a
lifetime feeding study with rats.
Teratogenicity / Reproduction Although there is some conflicting
evidence, most data indicate that diuron is not teratogenic. When
11-117
diuron was administered subcutaneously to mice at a level of 215 mg/kg
during days 6 to 14 of gestation, no significant increase was noted in
malformations among the offspring of treated mothers (USDHEW, 1969).
In another study, groups of pregnant Wistar rats were given 125, 250,
®
or 500 mg Karmex /kg on days 6 to 15 of pregnancy via gavage. The
Karmex formulation, which contained 80% diuron, was suspended in
com oil. No signs of maternal toxicity were seen, but maternzd body
weight was significzintly reduced in the 500 mg/kg dams. When rats
were killed on day 22, incidences of viable, dead, and resorbed fetuses
were comparable to controls. Mean fetal weight, however, was signifi-
cantly reduced in the top treatment level. An increased frequency in
the number of anomalous fetuses was noted at the 250 mg/kg level, but
not at 500 mg/kg, when compared to controls. The sole anomaly of
statistical significance was an increase in wavy ribs in the top two
treatment levels (4.3% and 4.8% for the 250 and 500 mg/kg groups,
respectively, compared to 1.5% for controls) (Khera et al. , 1979).
No terata were found in two multi- generation rat studies at a dietary
concentration of 125 ppm diuron (used in both studies) . A weight
depression in the second- and third-generation pups was noted in one
of the studies (EPA, 1981b; no additional data were available).
Mutagenicity As indicated in Table 11-33, diuron does not appear to be
a mutagen, although a positive finding with the addition of liver
enzymes indicates that further study is needed.
Summary An evaluation of important toxicity data is provided at the
end of this chapter.
11-118
TABLE 11-33
MUTAGENICITY TESTS: DIURON
Test System
Micronucleus test
Mouse bone marrow
Saccharomyces
cerevisiae mitotic
gene conversion
Saccharomyces
marcescens
Ames / Salmonella
Result Comments
Ames spot test
Salmonella
typhimurium G46
Escherichia coli WP2
Bacillus sub tills
"Rec" assay
rll mutants of T.
4
bacteriophage
Inhibition of testicular
DNA synthesis in
mouse +
Pelargonium z on ale
2000 mg/kg orally
100 yg /plate plus
liver in TA 1535
100 yl nitrosated
with sodium nitrite
in vitro then tested
100 yg
1000 mg/kg orally
10"^M
Source
Seller (1978)
Fahrig (1974)
Fahrig (1974)
Moriya et al. (1983)
Anderson et al. (1972)
Shirasu et al. (1976)
Seller (1978)
Seller (1977)
(
Moriya et al. (1983)
Shirasu et al. (1976)
Shirasu et al. (1976)
Anderson et al. (1972)
Seller (1978)
Pohlheim and Gunther (1977);
(
11-119
3. MOBILITY AND PERSISTENCE
Fate in Soil and Water
Diuron is considered a low mobility herbicide which remains near the
surface of the soil (Harris, 1967; Hill et al. , 1955; HoUings worth, 1955;
Miller et al., 1977; Mustafa and Gamar, 1972; Rhodes et al. , 1970). In
a review of 40 pesticides. Helling (1971a,b,c) found that diuron has low
mobility. Majka (1976) determined distribution coefficients to be 14.3
on silty clay loam and 6.5 on loamy fine sand. Both indicate very low
mobility. The retention of diuron in soil is suggested by its low
solubility (4.2 mg/100 ml water at 25°C--Ouellette and King, 1977), and
by the fact that diuron competes successfully with water for adsorption
sites in soil, particularly on organic matter (Hance, 1965a).
Lateral and vertical movement of diuron was studied by Ashton (1961)
on a peaty much, clay, and sandy loam. In all cases there was limited
lateral movement (distances not provided) and vertical movement was
restricted to the upper 2.5 cm of soil. Lateral movement was greatest
in the sandy loam and least in the peaty muck. In a field study,
diuron applied to the surface of a silty clay loam did not move below
the 0-5 cm layer after elution with up to 20 cm of water after 54 days
(Majka, 1976)
When Reed, (1982) applied 5.66 kg /ha of diuron to a silty clay loam
and a sandy loam low in organic matter, diuron remained in the 0-5
layer of soil through out the length of the test (23 days) (amount of
water applied not given). Pipe and Cullimore (1980) found that when
diuron was added to a heavy clay soil (pH 7.7) at a concentration of 1
ppm, most of the diuron (77%) remained in the top 2 cm, (time not
specified) .
Other trials, however, have shown higher movement. Ivey and
Andrews (1965) showed that phytotoxic concentrations moved 5-10 cm in
a Boudre clay loam (3% organic matter) and a Cumberland loam (2.2%
organic matter). Increased mobility occurred in soils with less organic
matter: phytotoxic concentrations reached 15 cm in a Collins silt loam
(1.1% organic matter) and a sequatchie fine sand (1.6% organic matter).
11-120
Reed (1982) found movement to 9 cm 8 weeks after application of diuron
applied at 5.66 kg/ha. At a higher appUcation rate (13.14 kg/ha) she
found movement down to 10-30 cm in a silty loam, a sandy loam, and a
sandy loam high in organic matter.
Limited information suggests that diuron may be somewhat persistent in
soils. In a study by the Department of Navy (1976) in which diuron
was applied at 1-2 kg /ha, the herbicide persisted for 4-8 months. In a
study by Ehman and Birdsall (1963), diuron persisted for 5-7 months
after application at 2-4 kg /ha (no specification of soil or definition of
persistence was provided for either of these studies). After diuron
had been applied 32 cotton fields every year for 4-8 years, no
phytotoxic residues were found one year after the last application
(Dalton et al., 1966).
Diuron is susceptible to microbial breakdown (DcJton et al. , 1966;
Geissbuhler et al. , 1975; Murray et al. , 1969). It is possible that
microbial breakdown is retarded by adsorption of diuron to soil parti-
cles. Geissbuhler et al. (1963) found that desorption of diuron in a
humus soil was too slow to maintain a constant rate of degradation by
bacteria. Metabolites identified in this study included N-(4-chloro-
phenoxy ) -phenyl- N-methylurea , N- ( 4-chlorophenoxy ) -phenylurea , and
( 4-chlorophenoxy ) -aniline .
In regard to runoff losses, two studies found only trace amounts of
diuron in drainage water (Rogers et al. , 1974; Willis et al. , 1975) (no
additional information provided) .
Fate in Water
The amount of diuron which will be adsorbed onto aquatic sediments was
found to be positively correlated with the amount of organic matter in
the sediments (Peck et al. , 1980). With high organic matter (for
instance, in most wetlands) more diuron is adsorbed, and the diuron is
more tightly held. In sediments which are low in organic matter,
diuron is readily desorbed. The study also found that there is
increased adsorption of diuron in bacterial and fungal cultures were
11-121
isolated from pond water and sediments which could degrade diuron. In
the laboratory, the mixed cultures could degrade 67%-99% of added
diuron. The major metabolite was 3, 4-dichloroaniline. (Ellis and Camp-
er, 1982)
Indicators of Potential Ground Water Contamination
Table 11-34 provides information on parameters associated with the
mobility of diuron. These parameters, and their associated thresholds,
have been suggested by EPA for use in assessing the potential for
pesticide contamination of ground water. A discussion of these
parameters and thresholds, and the methods for arriving at designated
values for individual herbicides, is presented in the main body of the
report as part of the discussion of the fate of herbicides in the
environment.
TABLE 11-34
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
DIURON
Indicator
Value for Diuron
Threshold
Solubility
42 ppm at 25°C
>30 ppm
K
oc
400
<300-500
Speciation at pH 5
ND*
Anionic
(negatively charged)
Hydrolysis half-life
Stable at pH 6-9
>6 months
Photolysis half -life
ND*
>3 days
Vapor pressure
3.1 X lO"^ mm Hg
<10~ mm Hg
*ND = no data
11-122
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Diuron appears to be non-toxic to test birds. Data available are LC-^
or LD Q values from Heath et al. (1972), Hill et al. (1975), and Tucker
and Crabtree (1970), The LC-^ values for mallard ducks, bobwhite
quail, Japanese quail, and ring-necked pheasants ranged from 1730 ppm
to greater than 5000 ppm, and the LDcn value for mallard ducks was
greater than 5000 ppm.
Fish
No information was found on the toxicity of diuron to fish.
Lower Aquatic Organisms
Pons and Pussard (1980) reported that 23 strains of amoebae showed no
toxic effects when treated with diuron. However, a number of cyano-
bacteria, green algae, and diatoms were reported to be sensitive to
diuron. An abstract by Bednarz and Zarnovski (1980) reported species
of Anabaena, Spirulina, Chlorococcum, Chlorella , and Ankistrodesmus to
be totally inhibited by 0.1 mg/1. A study by Pipe and CuUimore (1980)
showed a population decrease of 99% when the genera Oscillatoria,
Chlorella, Stichococcus , Hantzschia, and Navicula were treated with 1
ppm of diuron.
Soil Microorganisms
One study by Chandra et al. (1960) stated that diuron depressed the
microbial production of carbon dioxide in a number of different soil
types .
Toxicity Data Evaluation
The available carcinogenicity data are insufficient to assess diuron's
carcinogenic potential. In their registration standard review, EPA
found no studies on the carcinogenicity of diuron which met its require-
ments; two such tests have been requested by the agency from the
manufacturer. Conflicting results in the available data on teratogenic
effects do not allow any conclusion to be drawn. Two additional tera-
togenic tests have been requested by EPA, In regard to mutagenic
11-123
effects, the data in Table 11-33 suggest that diuron is not mutagenic,
although further tests are needed, as stated above. Three mutagen-
icity tests are required by EPA's registration standard: a gene muta-
tion study, a chromosomal aberration study, and a study on some other
mechanism of mutagenicity. Other toxicity data deficiencies identified
by EPA include an acute inhalation test and a dermal sensitization test.
No studies in EPA's registration files on diuron were conducted by IBT.
11-123. 1
I. GLYPHOSATE
1, INTRODUCTION
Glyphosate is the common name for the herbicide (N-phosphonomethyl)
glycine from Monsanto Chemical Company (Thomson, 1975). It is also
®
called by the trade name Roundup , a formulation that includes a
surfactant (MON 018). Glyphosate has the chemical structure shown
below.
0 0
HO-C~CH2-NH-CH2-P-OH
OH
Relevant chemical and physical properties are presented below in the
discussion of the fate of glyphosate in soil and water.
2. TOXICITY
Acute Toxicity
A low order of toxicity for glyphosate is indicated by acute oral and
dermal toxicity studies. Acute oral LDrn values for rats, mice, and
rabbits are 4320 mg/kg, 4873 mg/kg, and 3800 mg/kg, respectively
(Thomson, 1975; Ouellette and King, 1977; and MACC, 1982). Single
dermal dosages of 7940 mg/kg did not affect the survival of rabbits
(Spurrier, 1973).
Moderate toxicity is indicated by glyphosate when administered
intraperitoneally. The LDcq values for this route of exposure are 238
mg/kg and 134 mg/kg for rats and mice, respectively (MACC, 1982).
11-124
®
Severe eye irritation is observed in rabbits exposed to Roundup for-
mulations. In regard to skin irritation, glyphosate itself does not appear
to be a skin irritant. However, a mild skin irritation was seen in rabbits
®
after exposure to some formulations of Roundup (Spurrier, 1973, no data
provided). "^ - ~ -'
Mammalian Metabolism
According to a study obtained from EPA registration files (EPA, no
publication date provided [d]), glyphosate appears to be readily elimi-
14
nated. After rabbits were given a single oral dose of C-labeled gly-
phosate, more than 80% of the label was found in feces, and 7-11% was
found in urine within 5 days after treatment. Less than 10% was found in
expired air. Most of the remsdning label was located in the colon.
Special Studies
Monsanto (1982) reports that no signs of carcinogenicity, teratogenicity,
or neuropathology and no adverse reproductive effects from glyphosate
were seen in a 2 -year rat study, an 18 -month mouse study, and a 2 -year
dog study.
A number of studies have been published on the mutagenic potential of
glyphosate. As summarized in Table 11-35, most of these studies indicate
that glyphosate is not a mutagen. Two studies show questionable positive
responses. One of these, by Vigfusson and Vyse (1980), showed some
sister chromatid exchange upon exposure of human lymphocytes to rela-
tively high concentration of 0.25 mg/ml, 2.5 mg/ml and 25 mg/ml glypho-
sate. No clear dose response was evident. Furthermore, only two
donors were used for lymphocyte samples. Lymphocyte sister chromatid
exchange is known to vary considerably between subjects. The other
positive result came from an Ames/ Salmonella spot test in which exposure
to nitrosated glyphosate resulted in a slight increase in mutations at 1 yl
and 10 ul, but not at 100 ul (Seller, 1977). The author does not state
whether the lack of response at 100 pil is due to toxicity or to a poor
dose response.
Summary An eveiluation of important toxicity data is provided at the end
of this chapter.
11-125
ID
CO
I
CQ
<
H
<
O
o
H
w
w
H
H
I— (
O
i-i
w
o
<
H
D
u
nt
h
■4J
(0
^
<v«.k
c«
o
00
1—1
CO
1— 1
00
O^
1— 1
rH
0)
CO
s-*
^•^
m
rt
>
• 1-4
bO
00
1— 1
rt
•1— >
^ -#
-a
Z,
§
•
'O
"0
-^
rt
c
nS
•*-»
o
<u
c
(0
C
rt
(U
en
rt
(i
a
l-H
•rH
o
o
3
1— t
rt
a
o
o
w
>
o
2
^
CO
c
X
0)
(U
s
■*->
E
a;
o
(U
U
w
3
(0
CO
00
C7^
I— <
^-^
^^^
•
r-
n{
c^
o>
•4-)
(U
rt
>>
•i-i
1— 1
•IH
>H
a>
O
w
S
0)
(U
E
^
ti
« 2
«
CO O
bO
bO
O CO
§
0
o
0,-^
(U
^
5^
I— 1
•4-»
c
rt
1—1
^Tv SI
a >
a
<u S 4>
^_ r— t
■'~~
a
tSO
bO
O •i-t
flj >-t >H
3. CO
3
p.
CO
3
in 1— t
in
f— 1
QJ •1-4 •IH
CM a
<M
a
W c C
rt
c o
••-' I.
E
CO
H
(0
H
(D
.■::
bO >
q
rt
c
,c
• rH
o
CO
0)
(U
4-»
>>
73
o
•f-i
■♦-»
o
B
a
o
E
u
>>
A
1— 1
u
c
u
:i
(1)
B
CO
3
•1-*
X
in
13
1
rt
rt
x-^
?:5
<u tt
(U
coii
C
o
rt
r— (
>
E
J
• ft
rt
0
CO
O
u
CO
CO
m
o
CO
E
p
<
vO
^
'^t*
V
O
E
S
:3
(U
• rH
4->
u
rt
;3
E
CO
PU
u
• rH
J3
^
C
•M (X
• iH
• rH
CO >,
CO
(U ^.^
0
0)
+J
CJ
CO
4.^
O "Tt
• pH
CO '-'
■•->
o
•7-t
0)
mes
Salm
u
(U
rfl
CO
u
Pu
<
W
*
3. MOBILITY AND PERSISTENCE
Fate in Soil
Glyphosate binds tightly to soil particles (TRW, 1981). Helling
(1971a,b,c) states that glyphosate is readily adsorbed to all soils, and
that it is classified as immobile by the Helling and Turner classification
system. Adsorption of glyphosate begins immediately on contact with
the soil, and binding is rapid onto clays (kaolinite, illite, and ben-
tonite) and muck. Monsanto performed soil column leaching studies in
which soil columns were treated with glyphosate or its sodium salt and
then aged for 30 days (EPA, no publication date provided [d]). Upon
elution with 0.5 acre-inch of water for 45 days, the leaching of
glyphosate was said to be insignificant.
Adsorption of glyphosate is affected by a number of factors.
Phosphates compete with glyphosate for binding sites, so adsorption is
greater in low-phosphate soils (Sprankle et al. , 1975a). Adsorption is
greater in Fe and Al saturated soils than in Na or Ca
saturated soils. As would be expected, glyphosate was found to be
less tightly bound to sand than to other soils (Sprankle et al. , 1975).
A review by TRW (1981) concludes that glyphosate dissipates rapidly in
soil. In a study of microbial degradation, Reuppel et al. (1977) found
that glyphosate was degraded almost as rapidly as sucrose. When both
were labeled, 47% to 55% of the glyphosate radioactivity was given off as
C0„ in 4 weeks, compared to 57.9% for sucrose. This study found the
major soil metabolite to be aminomethyl phosphonic acid (AMPA).
Several other metabolites were also detected, all at less than 1% of the
original glyphosate concentration. These degradation products include
N-methylaminomethyl phosphonic acid, glycine, N , N-dimethylaminomethyl
phosphonic acid, and hydroxymethyl phosphonic acid. Rueppel et al.
(1977) state that based upon shake tests, AMPA is highly
biodegradable, although the rate may be slower than that of glyphosate,
possibly due to tighter binding to the soil and/or lower permeability
through the microbial cell walls.
11-127
Other information suggests a more variable persistence. Reuppel et al.
(1977) studied the dissipation of glyphosate on a silty clay loam, a silt
loam, and a sandy loam. When glyphosate was applied to the three
soils at rates of 4 ppm and 8 ppm, the half-lives on the three soils
were found to be 3, 27, and 130 days, respectively, independent of
application rate. Studies by Monsanto and others (EPA, no publication
date provided [d]) report half-lives in a variety of soils ranging from 8
to 19 weeks.
Reuppel et al. (1977) performed runoff potential experiments using a
silty loam, a silty clay loam, and a sandy loam in soil beds inclined at
an angle of 7.5°. Glyphosate was applied to the upper third of the
soil surface at a rate of 1.12 kg /ha. When artificial rainfall was applied
(amounts not given) at 1-, 3-, and 7-day intervals, it was shown that
the maximum runoff that would occur would be less than 0.02% of the
origincd herbicide applied.
Persistence in Water
There have been very few studies concerning the persistence of
glyphosate in water. The data suggest that glyphosate is slowly
degraded in aqueous systems. In a study by Brightwed and Malik (no
date provided), 0.1 ppm glyphosate was added to water samples from a
sphagnum bog (pH 4.23), a cattail swamp (pH 6.25), and pond water
(pH 7.33). After incubation in the dark for 49 days, the half-lives of
glyphosate were calculated to be 7, 9, and 10 weeks, respectively.
Serdy (1980) states that glyphosate is adsorbed to mineral and organic
matter and degraded by microorganisms.
Indicators of Potential Ground Water Contamination
"Table 11-36 provides information on parameters associated with the
mobility of glyphosate. These parameters, and their associated thres-
holds, have been suggested by EPA for use in assessing the potential
for pesticide contamination of ground water. A discussion of these
parameters and thresholds , and the methods for arriving at
designated values for individual herbicides, is presented in the main
11-128
body of the report as part of the discussion of the fate of herbicides in
the environment.
TABLE 11-36
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
GLYPHOSATE.._
Indicator
Value for
Glypho
sate
Threshold
Solubility
12,000 ppi
■n at
25'
°C
>30 ppm
K
oc
ND*
<300-500
Speciation at pH 5
Anionic
Anionic
(negatively charged)
Hydrolysis half-life
ND*
>6 months
Photolysis half-life
ND*
>3 days
Vapor pressure
Negligible
<10~ mm Hg
*ND = no data.
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
One feeding study by Serdy (1980) showed glyphosate to be non-toxic
to mallard ducks and quail, with LC_- values of greater than 4600 ppm.
Fish
A study by Folmar et al. (1977) found that the 96-hr LC__ values for
Roundup ranged from 2.3 mg/1 for fathead minnows to 13 mg/1 for
channel catfish (see Table 11-37). The data presented in this table
suggest that it is the surfactant (MON 0818), not the glyphosate, that
®
is the primary toxic agent in Roundup .
11-129
(D
C"-
o
5 -^
0)
CO
I
<
O
H
W
H
<
O
ac
>^
o
fa
o
H
1—1
u
I— I
X
o
E
(0
e
:3
0)
U 2
•^ C
o u
O tip
in in
^ -a
0)
h
u
(«
u
:3
8
1— 1
o
o
w
fa
I
vD
0)
U
c
0)
*^ o^
>o
00
o t-
c- •
I— I (VJ
I I
' fs3 o in
r"* o I— 1 1— I
^ ^ o o
CM
(M ro
(M
(0
a
o
IS
00
0)
u
E
l-H
o
fa
o
CM
I
I CM
I— I o^ r- I— I
c^ o
OS .
>
CM *5n CM (M
CM CM (M
o
vO
(— I
I
1—1
r-l
m
o
1—1
I
o
I
o
en ""^
o
o r-
O^
^-N r-
o
^-s.
1—4
•
r- •
•
o •
I— 1
nO
00
1
1— 1 CM
1 1
CO
CM r-i
1— 1 1
1— 1
t
CO
1
1
1— 1
CO
O nO
o
1 CM
1
rH
o
in
•
CM •
•
ON .
1— 1
•
rH
vO
r-l rH
<Na
C^ I-l
r^
1— 1
00
^-^
■*.• «-•
"^ — '
^-'^— '
*— '
*— '
•^
in
O i-l
-^
>• -"^r
CO
o
00
f— 1
•
"^J* .
•
a- .
1—1
CO
1—1
r-
i-l CM
rj
1—1
1—1
CM CM CM
CM CM CM
o
■♦->
E
u
o
fa
(0
(U
•IH
u
a
w
a
'a
c
o
Pi
3
o
»4
o
Pi
<U -M
®
a
:3
@
a
9)
••->
@
a
3
a;
•M
rt
(0
•4^
■4^
o O
TJ
T3
o
u
T)
0
o
X a
C
C
,c
(ti
c
^
n)
Glyp
Surf
3
3
a
3
a
M-l
0
O
>^
0
^
PJ
Pi
1— <
o
Pi
o
^
,i3
o
m
c
c
+J
• IH
rt
E
o
-a
•
i— 1
0)
<u
fa
o
a
V
ffi
en
n
fa
*— s
Q
O
H
H
P
H
<
2:
OT
o
O
u
E
>^
P^
tH
1
O
(-H
l-H
fa
U
O
pa
<
t— 1
H
U
n
X
o
H
>— ' ■*->
° §
o U
in
c
0)
u
h
O
^4
I
C3^
»4
I
(NJ
o
^ E
H
1-1
d
>my
T3
•
0
13
£
4^
^
^
^
0)
^
c
o
u
C
a
(d
B
1—1
in
o
O
fa
2
^^
^_^
^_^
^^
^^
o
vO
o
O
c^
•
•
•
vO
•
1
1
in
1—1
I
en
1
CO
1
00
CVJ
1
o
1
in
o^
•
•
•
1— 1
•
•
o
m
m
r— 1
(M
CO
^^
^-'
^^
■^^
in
o
o
O
O
•
•
•
^
•
t-
in
'^^
pH
m
o
^-^
vO
^
o
c^
t— 1
•
00
1
•
in
1
1—1
•
CO
1
1
1
00
1
->*
o
1
in
•
•
ro
•
c^
•"^l
en
1— t
(M
^^
■^-^
*— '
nO
•
en
•
o
in
O
•
o^
vO
TT
1—1
m
vO 1-1
(M
CM
(NJ
(NJ
(Na
(NJ
>
o
2
C
>
bO
o
2
(U
>
00
o
2
CO
rH
I
o
•IH
•4-»
(Ti
I— I
E
o
fa
0) ^
osat
ctan
C
^ (ti
3
0- t^
0
Pi
O W
®
@
a
a
3
13
T3
T3
C
C
3
3
O
O
Pi
pci
-a
o
(0
•iH
y
(U
00
(U
S
^
CO
-M
p-
:3
h
•4-J
o
(«
(tJ
Vh
u
O
H
Folmar et al. (1977) also exposed rainbow trout and channel catfish to
®
Roundup at various stages of development. For both species, the egg
®
stage was least sensitive to Roundup , and sensitivity increased in the
sac fry and early swim-up stages, then decreased as the fishes aged.
Trout eggs exposed to 10 mg/1 showed a significant reduction in the
percentage of eggs that hatched. No significant difference was noted
at 5 mg/1. A significant number of sac-fry were killed at 5 mg/1, but
®
not at 2 mg/1. The author concluded that applications of Roundup
could have adverse effects if applied when young fish were present.
In the material safety data published by Monsanto (no publication date
provided [a]). Roundup was referred to as being slightly or moder-
ately toxic to bluegill, carp, catfish, fathead minnows, and trout. The
LC-_ or TLj.- values ranged from 3.9 mg/1 for carp to 16 mg/1 for
catfish. Monsanto also reports that carp were unaffected for a period
®
of 90 days following exposure to an aerial application of Roundup at
the intended use level in a static pond.
Higher temperatures increase the toxicity of glyphosate to fish, as
®
shown in Table 11-38. Roundup is about twice as toxic to rainbow
trout at 17*^C as at 7°, and it is more toxic to bluegills at 27° than at
17° (Folmar et al. 1977). The effect of pH is less clear. Increasing
pH results in a decrease in the toxicity of glyphosate alone. Increasing
®
pH, however, results in a decrease in toxicity of Roundup or the
surfactant alone.
Lower Aquatic Organisms
As summarized in Table 11-39, the effects of glyphosate and its formu-
lations were investigated by Folmar et al. (1977). The 48-hr LC-- or
ECr^ values for Roundup range from 3.0 mg/1 for daphnids to 60 mg/1
for scud. The data indicate that the surfactant was more toxic than
the glyphosate in Roundup .
In the material safety data published by Monsanto (publication date not
®
provided [a]), Roundup was referred to as moderately toxic to
11-132
(4
oo
m
I
<
w
l-H
o
H
H
<
O
o
o
H
l-H
O
l-H
X
o
H
O
W
Pi
H
<
P£i
0^
w
H
O
H
U
w
tt,
fa
w
CO
to
e
o
o '^
O o^
in
<U
o
u
o
CO
I
vO
I
U
nJ
J
'o
fa
vO
"^
H
o
cr^
o
nO
o
•
•
•
•
•
1
00
1
xO
in
CO
•
(NJ
1
CO
00
CM
>£>
nO
vO
•
CO
•
CO
^"^^
V— ^
-s^^
N„^
in
•^
un
o
o
•
•
•
•
•
t>-
r^
r-
in
■^
""^
r— )
o
•
1
o
•
r— 1
•
CO
1
•
in
1
l-H
CO
•
1
1
00
1
1— 1
in
•
CO
CO
r^
■
vO
•
CO
CO
CM
0
O
(0
•l-l
o
a
CO
o
• l-H
(30
r-H
ti
rt
0)
o
G
{
<u
o
)h
u
(D
^
E
o
o
W
(X4
(0
o
CO
w
►— I
<
O
O
U
n
H
<
a
<
o
o
H
W
H
<
O
o
o
H
I— I
O
(— I
X
o
»4
^
(0
1
•*-»
vO
•s
O^
S
^^^
• IH
1-H
1— 1
bO
(U
^
o
o
73
^
IT)
«
X
U
C
1
J
o
u
00
u
0
in
o
<T-
in
J
13
H
(4
1
V4
■♦->
ni
U
o
E
H
oo
ro
CO
o
o
o
CO
CM
o
CO
CO
CM
00
(VJ
"<*
1
CO
(M
1
CO
o
Tj<
1
f-H
»
^
•
I— I
•
in
CO
00
CO
in
■ ^
CO
o
o
<\3
(M
<M
(M
(M
>
•1-1
O
2
c
0
p4
e
e
@
*J
a
a
a
iS
5
3
3
9
XI
T3
73
E
c
C
C
s
3
3
o
o
o
O
'J4
Pi
Pi
PJ
(0
o
a
o
c
■♦J
u
•T3
O
o
2
73
3
O
PJ
o
in
U
W
u
I
00
"^
(n
T3
0)
(0
CO
0)
a
X
0)
CO
u
Q)
cd
>
n
V4
T)
1—4
•l-l
C
^
TJ
bi:
a
3
73
rt
o
•rH
Q
W
2
(0
«
C
^
42
rt
D-
>H
rtJ
U
P
o
bC
Daphnia (the 48-hr LCj.. was 5.3 mg/1) and practically non-toxic to
crayfish (the 96-hr LC was >1000 mg/1).
Bees
Glyphosate appears to be non-toxic to bees. An experiment with bees
by Serdy (personal communication) indicated an LDrr, of greater than
100 yg/bee. Spurrier (1973) reported that honeybees could tolerate up
to 100 yg/bee for 48 hours (topically or orally). No study was cited.
The same data were reported in material safety data published by
Monsanto (date of publication not given).
Soil Microorganisms
A report by Reuppel et al. (1977) concluded that glyphosate appeared
to have no effect on the total microflora population. Quilty and
Geoghegan (1976) found glyphosate to have a minimal effect on
microflora in peat. A review of registration files by the EPA (no
publication date provided [d]) concluded that glyphosate showed no
apparent effect on nitrification or nitrogen fixation by microbes, or on
degradation of starch, cellulose, protein, or leaf litter.
Bioaccumulation
In the material safety data published by Monsanto (no publication date
provided [d]), tissue residue analyses indicated that glyphosate does
not bioaccumulate in carp exposed for 90 days to an intended use level
®
of Roundup aerially sprayed on a static pond. Similar conclusions
were drawn by Monsanto (no publication date provided [b])). A study
by Folmar et al. (1977) reported the effects of exposing rainbow trout
to 0.02, 0.2, and 2.0 mg/1 to the isopropylamine salt of glyphosate or
®
Roundup for 12 hours. No residues were found at the two lower
concentration, but at at the highest level, (2.0 mg/1), fillets contained
80 yg/kg and the eggs contained 60 yg/1 of glyphosate.
Monsanto (1982) states that glyphosate's high water solubility and low
lipid solubility suggests that it should not bioaccumulate and that it
should not accumulate in the event of repetitive exposure.
11-135
Toxicity Data Evaluation
Most of the concern about data regarding glyphosate toxicity has
focused on the tests done by IBT. The following studies done by IBT
on glyphosate were determined to be invalid and have been replaced by
Monsanto:
dermed (rabbit) subchronic (3 studies)
chronic oral (rat)
carcinogenicity (mouse)
mutagenicity (mouse)
teratology (rabbit)
mutagenicity (Ames test)
recombination assay
teratology (rabbit)
subchronic inhalation (rat)
dermal (rabbit)
The following studies were found to be valid:
reproduction (rat)
subchronic oral (rat)
subchronic oral (dog)
chronic oral (dog)
mutagenicity (rat/ mouse)
reproduction/ residue (hen)
dermal (qucdl)
dermal (swine)
dermal (cattle)
dermal (hen) (2 studies)
EPA has decided that a subchronic oral (rabbit) and a cholinesterase
(rat) study are no longer required. The agency is still reviewing a
pilot cind chronic feeding study (rat) and a chronic oral (dog) study.
Monsanto has given EPA a negative response in regard to its intention
to replace a mutagenicity study (mouse) and a teratology study (rab-
bit) . The company has not yet responded in regard to its intention to
replace a reproduction (rat) study.
11-135. 1
More publicly available information is needed to allow an independent
review of glyphosate. Because glyphosate was registered since the 1972
data requirements, however, it can be assumed that, once the IBT data
replacement is completed, the full complement of data will have been
reviewed and found acceptable by EPA.
11-135. 2
J. KRENITE
1. INTRODUCTION
®
Krenite is the trade name for the herbicide ammonium ethyl carbamoyl
phosphonate, produced by E. I. du Pont de Nemours and Company
(Thomson, 1975). Its common name is fosamine ammonium, and its
structure is
0 0
II II
CH3CH2-0-P-C-NK
0NH4
®
Krenite contains 41.5% fosamine ammonium (4 lb /gallon) (Du Pont,
1983). Relevant physical and chemical characteristics are presented
®
below in the discussion of the fate of Krenite in soil and water.
2. TOXICITY
Acute Toxicity
®
Krenite appears to have low acute toxicity. Toxicological information
supplied to Du Pont by Sherman (1979) cited oral LD_-. values for the
42% aqueous solution of the active ingredient, fosamine ammonium, to be
24,000 mg/kg for male rats, 7,380 mg/kg for guinea pigs, and >15,000
mg/kg for female beagle dogs. Sherman (1979) studied dermal toxicity
and reported that a maximum feasible dose of 1680 mg/kg resulted in no
signs of toxicity in New Zealand rabbits. The USD A (1978) reported an
acute dermal LC^^ value for fosamine ammonium to be >4000 mg/kg for
rabbits .
In regard to inhalation toxicity, Sherman (1979) found that fosamine
ammonium concentrations of 56.6 mg/1 and 42.0 mg/1 showed no signifi-
11-136
cant clinical signs of toxicity to female rats exposed to 1 hour of the 42%
aqueous solution in aerosol form. In a test for eye and skin irritation,
New Zealand rabbits exposed to 10 ml of the 42% aqueous solution showed
mild to moderate erythema after a 24-hour exposure, but after 72 hours,
appearance was normal. New Zealand rabbits showed no ocular effects
when exposed to 0.1 ml of the 42% aqueous solution of fosamine ammonium
24, 48, and 72 hours after treatment (Shermetn, 1979).
Fosamine ammonium formulations often contain non-ionic surfactants such
as Tween 20®, Triton X-100®, or Du Pont Surfactant WK®. OSHA data
sheets and information supplied by the manufacturers state that these
materials are not considered hazardous or toxic (TRW, 1981).
Special Studies
Carcinogenicity No data are available.
Teratogenicity/ Reproduction Sherman (1979, unpublished; no data pro-
vided) fed 0, 200, 1000, and 10,000 ppm fosamine ammonium to Charles
River-CD rats on days 6 through 15 of gestation. No signs of embryotox-
icity or teratogenicity were observed, based on the absence of internal,
skeletal, or external abnormalities or malformations.
Mutagenicity No indications of mutagenic potential were seen in an E. coli
WP2 test system and an Ames / Salmonella test system using strains TA-98
and TA-100 (Moriya et al. , 1983). Sherman (1979, unpublished; no data
provided) found no evidence of mutagenicity in an Ames / Salmonella test
using stredns TA-1535 and TA-100 to detect base-pair substitution muta-
tions and strains TA-1537, TA-1538, and TA-98 to detect frame shift
mutations .
Summary An evaluation of important toxicity data is provided at the end
of this chapter.
3. MOBILITY AND PERSISTENCE
Fate in Soil
Fosamine ammonium is considered to have low mobility in soil, despite
its high water solubility (179 g/lOOg; no temperature given) (TRW,
11-137
1981). This is due to a strong tendency to adsorb to soil particles.
Fosamine ammonium was found to have a Freundlich equilibrium constant
of greater than 20 on Keyport silt loam (17% clay, 2.8% organic matter)
(Du Pont, 1975. A standard textbook on ground water movement
(Freeze and Cherry, 1979) states that a Freundlich equilibrium constant
of greater than 1 indicates that a substance is essentially immobile in
porous media (such as soil). EPA considers values greater than 1 to 5
as indicative of a low potential for ground water contamination
(Servern, 1983).
The potential for movement of fosamine ammonium was studied under
simulated rainfall conditions, using a sandy loam (12% clay) in a flat
(12" X 36" X 3") sloped at 5° -10°. Water was applied for 2 hours at a
rate of 12»5-25 ml/hr. The top third of the flat was treated with 15
lb /acre fosamine ammonium. Most (92.6%) remained in the first inch of
soil. TRW (1981) states that several other field studies (EPA
no publication date provided [b] ; Han, 1979b; Mullison, 1979), for
which no data are presented, also confirm that fosamine ammonium has a
low vertical mobility. Soils with higher adsorption capacities will tend
to retard fosamine ammonium movement more than soil with lower adsorp-
tion capacities. In a laboratory leaching test using silt loam (17% clay)
and a sandy loam (12% clay), fosamine ammonium moved more in the soil
with the lower clay content, although mobility was low in both soils
(TRV7, 1981; no primary source given).
Because fosamine ammonium tends to stay near the soil surface, erosion
or runoff may lead to lateral movement of the herbicide, especially after
a heavy rainfall (TRW, 1981; no primary source given),
Fosamine ammonium is not considered to be persistent in soils. It has a
half-life of approximately one week (Han, 1979b) to 10 days (Mullison
1979). Han (1979b) documented that 11.3 kg/ha of fosamine ammonium
applied to a silt loam (17% clay, 2.8% organic matter) had a half- life of
approximately 1 week. In a heavier silt loam (31% clay, 4% organic
matter) it had a half-life of less than 1 week. In two silt loams and a
fine sand, fosamine ammonium and its major metabolite carbamoyl-
11-138
phosphonic acid (CPA) were not detected after 3 to 6 months (Han,
1979).
Theoretically, fosamine ammonium can be degraded to CPA by chemical
hydrolysis (Han, 1979b; MuUison, 1979). However, Han (1979b) showed
that under sterile soil conditions fosamine ammonium was not degraded
in the first 20-30 days and only minimally thereafter. Under unsterile
conditions, degradation was fairly rapid (20%-25% of the original weight
14
of C was evolved in the first 20-30 days). Thus, it appears that the
degradation of fosamine ammonium in the soil is predominantly due to
microbial action.
When degradation rates were compared in two silt loams and a fine
sand, it was found that fosamine ammonium was metabolized to CPA more
quickly in the fine sand (Leon Immokalee fine sand, with 99% sand and
1% organic matter) , although the subsequent degradation of CPA was
somewhat slower in the fine sand than in the silt loams (Han, 1979b).
Persistence in Water
The degradation of fosamine ammonium in water appears to be strongly
pH-dependent (Han, 1979b). At a pH of 5, fosamine ammonium at 5
ppm was hydrolyzed nearly completely to CPA within 2 weeks, with a
half-life of approximately 10 days. At pH 7 and 9, the same
concentration of fosamine ammonium was found to be stable for 4 weeks
(less than 3% decomposition). These laboratory studies were conducted
in the dark, using labeled fosamine ammonium. The author concludes
that decomposition will be minimal under field conditions; however, the
slightly acidic nature of many Massachusetts waters may increase
decomposition .
Photolysis of fosamine ammonium appears to be minimal under both field
and laboratory conditions. At an aqueous concentration of 5 ppm at pH
5, photodegradation was "very minor" after 4 weeks in direct July
sunlight in Wilmington, Delaware (Han, 1979b). In a laboratory study,
when an aqueous solution of 5 ppm fosamine ammonium was irradiated at
11-139
an intensity of 1200 watts /sq cm, only 2% decomposition occurred after 8
weeks (Han, 1979b).
Indicators of Potential Ground Water Contamination
Table 11-40 provides information on parameters associated with the
mobility of fosamine ammonium. These parameters, and their associated
thresholds, have been suggested by EPA for use in assessing the
potential for pesticide contamination of ground water. A discussion of
these parameters and thresholds, and the methods for arriving at
designated values for individual herbicides, is presented in the main
body of the report as part of the discussion of the fate of herbicides in
the environment.
TABLE 11-40
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
FOSAMINE AMMONIUM
Indicator
Solubility
K
oc
Spe elation at pH 5
Hydrolysis half-life
Photolysis half-life
Vapor pressure
Value for
Fosamine Ammonium
Threshold
1,790,000 ppm
at 25°C
>30 ppm
ND*
<300-500
ND*
Anionic
(negatively charged)
2 weeks**
>6 months
ND*
4 X 10"^ mm Hg
at 25°C
>3 days
<10"^mm Hg
* ND = no data
** To CPA at 24° and pH 5.5-6.5.
11-140
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Studies by Mullison (1979) and E. I. Du Pont de Nemours Company
(1979) using mallard ducks and bob white quail showed fosamine
ammonium to have low toxicity for these species. The LD_ values for
both species were greater than 10,000 mg/kg.
A study by Sherman (1979) reported the acute LDr^ values for mallard
ducks and bobwhite quail to be greater than 5000 mg/kg for both
species of birds. The same report cited LCr-. subacute toxicities for
both species to be greater than 10,000 ppm.
Fish
Fosamine ammonium appears to be non-toxic to fish. A study by the
U.S. Department of the Interior (1978) showed fosamine ammonium to
have a low toxicity for bluegills, rainbow trout, and fathead minnows,
with LCp.^ values ranging from 670 ppm to greater than 1000 ppm. A
static bioassay by Du Pont (1980) on salmon indicated a 96-hour LC^.-
of 8290 ppm.
Lower Aquatic Organisms
One study by Du Pont (1980) shows fosamine ammonium to be non-toxic
to Daphnia, with a 48-hr LC_- of 1524 ppm.
Bees
Fosamine ammonium appears to be non-toxic to bees. A solution with
10,000 ppm produced no greater mortality than that seen in a control
population of bees, according to a study by Du Pont (1980).
Soil Microorganisms
Non-photosynthetic microorganisms seem to be relatively unaffected by
fosamine ammonium. EPA (publication date not provided [b]) state that
in three types of soils, populations of various bacteria and fungi
remained unaltered over a 8-week period after treatment with 10 ppm
fosamine ammonium. The same report showed little or no fungal toxicity
at rates up to 100 ppm when using various species of fungi (Aspergillus
11-141
niger, A. terreus, Penicillium citrinum , Gibberella aubinetti, Fusarium
sp., Altemaria sp., Rhizoctonia solani, and Pythium sp.). Soil-
nitrifying bacteria in two different soils remained unaffected during a
5-week period after treatment with 0.5, 5, and 20 ppm fosamine ammon-
ium in studies by Han (1979) and by Han and Krause (1979). How-
ever, Hallborn and Bergman (1979) reported that the rate of nitrogen
fixation by the lichen Pel tig era praetextata and its free-living phyco-
biant algae, Nostoc sp., was drastically reduced, with total inhibition
occurring after 8 hours.
Potential for Bioaccumulation
Moore (1976) reports that fosamine ammonium is considered to have a
low potential for bioaccumulation. Han (1979a) showed that fosamine
ammonium and its soil degradation product, carbamoylphosphonic acid,
did not accumulate in channel catfish when they were exposed to 1 ppm
fosamine ammonium for 4 weeks. The accumulation factor was less thcin
1, and 50% of these residues were eliminated after 2 weeks.
Toxicity Data Evaluation
More publicly available information is needed on fosamine ammonium.
However, since it was registered after the 1972 data requirements were
in place, it can be assumed that the manufacturer conducted the com-
plement of tests required by EPA at that time and that the results were
found to be acceptable by EPA. No tests were conducted by IBT.
11-142
K. METOLACHLOR
1. INTRODUCTION
Metolachlor is the common name for the herbicide 2-chloro-N- (2-ethyl-
6-methylphenyl)-N-(2-methoxy-l-methylethyl) acetamide. (American Na-
tional Standards Institute, 1976), produced by Ciba-Geigy Chemical
® ®
Company. It is also called Dual , Ontrack , and the experimental
number CGA-24705. It has the chemical structure
CH, *r"3
CH-CHj-O-CHj
CO-CHjCI
CH2CH3
Relevant chemical and physical properties are presented below in the
discussion of the fate of metolachlor in soil and water.
2. TOXICITY
Acute Toxicity
Metolachlor exhibits a low order of toxicity in acute tests. Bathe
(1973) reports the LD^.^ value for technical metolachlor for rats to be
2780 mg/kg. Several studies have been done of the 6 lb and 8 lb per
gallon emulsifiable concentrate (EC) formulations. The acute oral LD_-
dO
value for the 6 lb /gallon EC formulation was found to be between 2000
and 5000 mg/kg for rats by Affiliated Medical Research, Inc. (1974a).
Nham and Harrison (1977a) reported the LD__ for the 8 lb /gallon EC to
be 2530 mg/kg.
Low acute dermal toxicity was indicated in a study by Affiliated Medical
Research, Inc. (1974b) which found an LD_- of greater than 10,000
50 '^
11-143
mg/kg when technical metolachlor was applied to unabraded rabbit skin.
The same study found an acute dermal LDrn of one 6 lb /gallon EC
formulation to be also greater than 10,000 mg/kg. Nham and Harrison
(1977b) established the LD for rabbits to be greater than 3038 mg/kg
via the intact dermal route.
Low inhalation toxicity was found by Sachsse and Ullman (1974), who
observed no deaths of rats after a 4-hour exposure to 1.752 mg/1
(maximum achievable level) of the technical form,
Sachsse (1973a) found metoloachlor to be non-irritating (irritation index
of 0.1) when technical metolachlor was applied to the skin of rabbits.
Mild irritation (irritation index of 1.62) was observed for one 6
lb/gallon EC formulation by Affiliated Medical Research, Inc. (1974c).
Scribor (1977b) reported moderate erythema, edema, and second-degree
burns after a 72-hour treatment with the 8 lb /gallon EC formulation.
Technical metolachlor (0.1 ml) was found to be non-irritating to rabbit
eyes after 24 hours and after 7 days in a study by Sachsse (1973b).
Subchronic Toxicity
In their registration standard review of metolachlor, EPA (1980)
reported problems with a number of subchronic studies. One study
considered valid was performed on dogs for 6 months and showed that
metolachlor produced no observable effects at a dietary dose of 100
ppm. When 540 mg/kg/day of metolachlor 6E (68.5% a.i.) was applied
to the skin, no significant evidence of systemic effects was noted. At
1080 mg/kg/day, the only reported effect was decreased body weight
gain (Affiliated Medical Research, Inc., 1974d) .
Special Studies
Carcinogenicity In its registration standards review of metolachlor,
EPA (1980) cited two studies which showed no evidence that metolachlor
is a carcinogen, although further testing is needed. One study cited
by EPA (Gesme et al. , 1977) was conducted by Industrial Bio-Test
Laboratories (IBT) , and validated later by Ciba-Geigy and EPA after an
11-144
in-depth evaluation. The study showed no evidence of carcinogenicity
after feeding 50 male and 50 female Charles River CD-I rats at dietary
dosages of 30, 1000, and 3000 ppm metolachor. Although several
deficiencies in animal husbandry and good laboratory practices were
noted, EPA decided that the negative results were supported by the
raw data.
The other study cited by EPA (1980) is a 2-year feeding study on the
rat which also reported no evidence that metolachlor is carcinogenic
(Kennedy, 1976). These results, however, are considered only "supple-
mentary" by EPA, because of significant deficiencies in test protocol,
including a failure to verify the dose levels by an analysis of the diet.
Teratogenicity / Reproduction No fetotoxic effects or effects on offspring
were noted after 60, 180, and 360 mg/kg/day of metolachlor were
administered to female Sprague-Dawley rats during days 6 to 15 of
gestation. The only effect noted was a decrease in food consumption at
the highest dose in the early part of the experiment. A study by
Smith and Adler (1978) found no reproductive effects of metolachlor on
the rat. EPA considered the conclusions of the test to be only
"supplementary" information, because of several deficiencies in the test,
including problems in animal husbandry, mating performance and
success, and observation records.
Mutagenicity
Two tests cited by EPA (1980) showed no evidence of mutagenic activity
of metolachlor. Arni and Miller (1976) tested metolachlor in a bacterial
(Salmonella) system, utilizing activation by mammalian microsomes. No
increase in base substitutions or point mutations was observed in
comparison to controls at a range of 10, 100, 1000, and 10,000 yg /plate.
The effect of metolachlor on developing sperm was investigated by
Ciba-Geigy Limited (1976) in an in vivo mouse study using single oral
doses of 100 and 300 mg/kg metolachlor. No effect was observed on
fertility rates or on zygote or embryo survival. No malformations of
resulting embryos were noted.
11-145
Neurotoxicity Since metolachlor is a chloracetanilide herbicide, it is not
expected to cause esterase depression or delayed neurotoxicity (EPA,
1980), No test for neurotoxicity is required for metolachlor by EPA.
Summary An evaluation of important toxicity data is provided at the end
of this chapter.
3. MOBILITY AND PERSISTENCE
Fate in Soil
The information discussed below is from the EPA pesticide registration
standard for metolachlor issued in 1980, which reviews information sub-
mitted by the manufacturer as well as information which is publicly
available.
Metolachlor appears to have a significant potential for movement in soil.
Its water solubility is high (530 ppm at 20°C). In a column study done
by Houseworth (1973), "extensive leaching" of metolachlor was observed
in soils having a low percentage of organic matter. Dupre (1974a) and
Houseworth (1973) document that leaching will readily occur in sandy loam
and sandy soils that are low in organic matter (<2%) . In the latter
study, 20% to 33% of the applied metolachlor leached more than 30 cm (12
inches) in the soils when an equivalent of 20 inches of rainfall was
applied to a column that was overlain by metolachlor. Ballantine (1975)
showed substantial leaching of metolachlor and its metabolites (by ana-
erobic degradation) into the 6-inch to 12-inch soil horizon in five soil
types. In a study by Skipper, Gossett, and Smith (1976), extensive
leaching was considered to be the major cause of disappearance of meto-
lachlor from the upper 3 inches of a sandy loam soil (no data provided) .
In field dissipation studies (Ballantine, 1975) 2 and 4 lb a. i. /acre of
metolachlor were added to five soils: a "Mississippi loam," a "Nebraska
silt loam," and three unnamed soils from New York, California, and
Illinois. In the top 12 inches of soil metolachlor dissipated to 10% of the
original dose after 60 to 162 days. Part of this loss would be due to
microbial degradation, both aerobic and anaerobic (McGahen and Tiedje,
1978). In a clay loam, EUeghausen (1976a, b) found 90% degradation
under non-sterile conditions.
11-146
Degradation products may also be mobile. Dupre (1974b) reports that
"residues of aged 14-C-Metolachlor" were observed to leach in sandy
loam soil. The results suggested that several different chemicals were
involved, each with a different mobility.
Dupre (1974a) conducted a runoff study which indicated that both sheet
erosion and leaching are probably involved in the movement of
metolachlor (no supporting data provided) .
The hydrolysis half-life of metolachlor is 200 days over a pH range of 5
to 9, indicating considerable stability in regard to this route of
degradation. Photolysis may be more important, given a 50%
degradation in sunlit soil after 8 days (Aziz, 1974). However, EPA
(1980) considers photolysis to be an insignificant route of loss if
metolachlor is incorporated into the top 2 inches of soil. Volatility is
probably not a significant route of loss, since metolachlor has a vapor
-5
pressure of 1.3 x 10 mm Hg at 20°C.
At the end of the its discussion of the fate of metolachlor in soil, EPA
(1980) states that "This high mobility, in combination with a potential
for long-term environmental stability, may prove to be [a] significant
concern in projecting potential exposures to Metolachlor residues."
Fate in Water
The only data available on the fate of metolachlor in water concerns its
degradation by hydrolysis and photolysis, both of which are
insignificant. In buffered solutions at a temperature of 30°C and at pH
levels of 5,7, and 9, metolachlor was stable for 28 days (Burkhard,
1974). The percentages remaining at each pH level were 97, 100, and
96, respectively.
Aziz and Kahrs (1975) found metolachlor to be relatively stable in
aqueous solutions exposed to natural sunlight. After 30 days, only
6.6% of the original concentration had been photolyzed.
11-147
Indicators of Potential Ground Water Contamination
Table 11-41 provides information on parameters associated with the
mobility of metolachlor. These parameters, and their associated thres-
holds, have been suggested by EPA for use in assessing the potential
for pesticide contamination of ground water. A discussion of these
parameters and thresholds, and the methods for arriving at designated
values for individual herbicides, is presented in the main body of the
report as part of the discussion of the fate of herbicides in the
environment .
TABLE 11-41
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
METOLACHLOR
Indicator
Solubility
K
oc
Speciation at pH 5
Hydrolysis half-life
Photolysis half-life
Vapor pressure
Value of Metolachlor
530 ppm at 20°C
178.4
Cationic*
(positively charged)
>200 days**
Slow
(8% after 30 days)
1.3 X lo'^ mm Hg
at 20^C
Threshold
>30 ppm
<300-500
Anionic
(negatively charged)
>6 months
>3 days
-2
<10 mm Hg
* By analogy with trimethylamine .
** At 20"C and pH 5-9.
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Two studies by Fink assessing the effect of metolachlor on birds are
reported by EPA (1980) as part of their generic standards review.
Fink (1974a, b) reported dietary LD . values for mallard ducks and
bobwhite quail to be greater than 10,000 ppm, indicating that
11-148
metolachlor was practically non-toxic to upland game birds and
waterfowl.
Fink (1978a, b) also studied the effect of metolachlor administered for 1
week to quail and mallard ducks. At most dosages, significantly fewer
chicks survived to 14 days, as shown in Table 11-42.
Fish
EPA (1980) concluded that metolachlor was moderately toxic to fish.
One study by Buccafusco (1978a, b) reported 96-hr LC_« values for
bluegills and rainbow trout to be 10.0 ppm and 3.9 ppm, respectively.
Dionne (1978) found the no effect level, below which no effects were
observed, to be between 0.78 and 1.60 ppm.
TABLE 11-42
EFFECT OF METOLACHLOR ON REPRODUCTIVE SUCCESS OF BIRDS
Pesticide
Concentration
Significance
Species
(ppm)
% Survival
Level
Source
Mallard
duck
Control
57.0
Fink (1978b)
10
48.0
0.0001
11
300
57.6
NS
n
1000
51.0
0.025
n
Bobwhite
quail
Control
58.8
Fink (1978a)
10
47.0
0.001
II
300
37.0
0.001
n
1000
41.5
0.001
n
*NS = Not significant.
11-149
Lower Aquatic Organisms
Vilkas (1976) reported the 48-hour LC_- for technical metolachlor to be
25.1 ppm Daphnia magna. The 48-hr no-effect level was 5.6 ppm.
Based on these data, the EPA (1980) concluded that metolachlor was
slightly toxic to aquatic invertebrates.
Soil Microorganisms
Ercegovich et al. (1978a) studied the effect of metolachlor on 27 species
of microorganisms, including the genera Bacillus, Cellulomonas ,
Cytophaga, Flavobacterium , Pseudomonas, Achromobacter , Aspergillus,
Chaetomium , Fusarium , Penicillium, and Trichoderma. At 5 ppm
metolachlor, the polulation growth of 6 of 27 species was inhibited; at
25 ppm, 9 of 27 species were inhibited, with a static (but not cidal)
effect shown at both concentrations. The EPA (1980) concluded that if
metolachlor was applied as directed at 1-3 lb a. i. /acre, slight
inhibitory / static effects would be expected. The adverse effects would
lessen with time, and populations would be expected to recover.
Ercegovich et al. (1978b) studied the effect of 5, 25, and 125 ppm
concentrations on nitrification rates in Morrison sandy loam and
Hagerstown silt loam. Morrison sandy loam showed no effects at any
concentrations evaluated, and the Hagerstown silt loam showed inhibition
only at 125 ppm, which lasted for a 7-week period (recovery began at
week 8).
Bioaccumulation
One study by Elleghausen (1977) indicated that algae and Daphnia
accumulated 10.4 and 0.60 ppm when exposed to 0.1 ppm metolachlor.
An 8-hour period of depuration was needed for a 50% loss of the
accumulated metolachlor. Catfish (also exposed to 0.1 ppm) accumulated
1.20 ppm in a 96-hour exposure.
Smith (1977) and Barrows (1974) measured the bioaccumulation of
metolachlor in fish. The EPA (1980) concluded that both studies
indicate that metolachlor accumulates in fish.
11-150
Toxicity Data Evaluation
EPA, in its registration standards review of special studies using
metolachlor, stated that "although no positive evidence of general
chronic, teratogenic, fetotoxic, oncogenic, or mutagenic effects has so
far been presented, the available information is presently insufficient to
satisfy all the agency's requirements for the study of chronic effects."
Specifically, gaps identified in EPA's Registration Standard included a
mammalian oncogenicity study (other than one using a mouse) , a rat
chronic feeding study, a mammalian reproduction study, and a mamma-
lian teratology study (other than one using a rat) . The registrant has
submitted new data to satisfy these requirements; these studies are
currently being reviewed by EPA,
Several studies on metolachlor were conducted by IBT, EPA decided
that portions of two studies done by IBT on chronic oral effects and
reproductive effects are valid and could be used as supplemental infor-
mation. Both of these studies have been replaced by Ciba-Geigy.
Several chronic studies and one reproductive study done by other
laboratories already exist in EPA files. A carcinogenicity study done
by IBT is still under validation review.
11-150. 1
L. PICLORAM
1. INTRODUCTION
Picloram is the common name for the herbicide 4-amino-3 ,5,6-trichloro-
picolinic acid produced by Dow Chemical Company. It is also called
Amdon® (TRW, 1981), Borlin®, and Borolin®, and Tordon®. Tordon
lOK and Tordon 22K contain picloram only, while Tordon 101 contains
®
2,4-D, and Tordon 155 contains 2,4,5-T. Numerous other formulations
are available. Picloram can be applied as a spray solution to leaves or
stems, as pellets to the ground, or as a liquid injected into the tree or
painted on cut surfaces (TRW, 1981). The structure of picloram is
CI
NK
CI
.^^^C
<^
N
\
OH
Other relevant physical and chemical parameters are presented below in
the discussion of the fate of picloram in soil and water.
2. TOXICITY
Acute Toxicity
Acute toxicity tests indicate that picloram has a low order of toxicity.
The LDj.. values are 8200 mg/kg, 3000 mg/kg, and 2000 mg/kg in rats,
guinea pigs, and rabbits, respectively. In mice, the LDj.. values range
from 2000 to 4000 mg/kg (MuUison, 1979). Tordon 101® (a formulation
of picloram and 2,4-D) has an LD--. value of 3800 mg/kg in female rats
(Lynn, 1965). In rabbits, the dermsil LD-^^ value is >4000 mg/kg (U.S.
Forest Service, 1974). NRCC (1974) reports that picloram does not
appear to present an acute inhalation hazard, since no adverse effects
11-151
were seen in albino rats exposed for 7 hours to a saturated atmosphere
of the potassium salt of picloram. Additionally, no adverse effects were
seen after a 7-hour exposure to air that was bubbled through a solution
of Tordon 22K® (Lynn, 1965).
No skin irritation was observed when various concentrations of picloram
were applied to the skin of rabbits for several days. Rabbits exposed
dermally to undiluted picloram for 9 days exhibited only slight
exfoliation and hyperemia (U.S. Forest Service, 1974). Slight to
moderate conjunctival irritation resulted when the eyes of albino rabbits
were exposed to undiluted picloram. These effects cleared within a
week (NRCC, 1974). In addition, when undiluted picloram was applied
directly to the conjunctival sac of these animals, a slight redness and
corneal cloudiness appeared, but cleared within 1 to 2 days (Lynn,
1965).
Subacute Toxicity
The results of a 90-day feeding study with rats showed no apparent
adverse effects and 75 mg/kg (Lynn, 1965). No toxic effects were
observed at concentrations of up to 1000 ppm picloram. At 3000 ppm
picloram, the liver-to-body weight ratio in females was increased. At
10,000 ppm picloram, slight to moderate, unspecified pathological
changes of the liver and the kidney were noted. The organ-to-body
weight ratios for the liver and kidney were also significantly increased
(McCoUister and Lang, 1969). In a 6-month feeding study in which
Sprague-Dawley rats were fed 100 mg/kg of the potassium salt of
picloram, no adverse effects were observed. At 1000 mg/kg, females
showed a reduced growth rate and a significant increase in
organ-to-body weight ratios for the kidney, liver, and suprarenals. In
males fed 1000 mg/kg, a significant increase was observed in
organ-to-body weight ratios for kidney, liver, and testicles (Suschetet
and Causeret, 1973; Suschetet et al. , 1974). An 11-day study in which
diluted picloram was applied nine times to the skin of rabbits resulted
in slight exfoliation and hyperemia of the abdominal skin.
11-152
Mamalian Metabolism and Uptake
Picloram appears to be rapidly excreted from the mammalian system and
does not accumulate in tissues (McCoUister and Leng, 1969). These
14
authors report that 90% of carboxyl- C-labeled picloram fed to dogs at
a concentration of 97 ppm was excreted unchanged in the urine within 2
days.
Special Studies
Carcinogenicity The major study available on the carcinogenicity of
picloram was conducted the the NCI (1978) on rats and mice. In this
study, 50 male and 50 female Osborne-Mendel rats or B6C3F1 mice were
administered technical grade picloram at the maximcilly tolerated dose
and at one-half this amount for 80 weeks. These dosages (time-
weighted) were 7437 and 14,875 ppm for rats and 2531 and 5062 ppm for
mice. A disproportionately small number of controls (10 rats and 10
mice) were used in this study.
The authors concluded that picloram was not carcinogenic for B6C3F1
mice or male Osborne-Mendel rats, based on a statistically insignificant
incidence of malignant tumors. A statistically significant increase in
neoplastic nodules of the liver (benign tumors) was observed in rats,
along with treatment-related lesions of the liver diagnosed as foci of
cellular alteration. In addition, the results indicated a relatively high
but statistically insignificant incidence of follicular hyperplasia, C-cell
hyperplasia, and C-cell adenoma of the thyroid in rats of both sexes.
This study has generated considerable discussion. Part of this
discussion has concerned the significance of the benign neoplastic
nodules and the lesions diagnosed as foci of cellular alteration, in
relation to the potential for malignancy. The lesions of cellular
alteration have been commonly observed in association with the induction
of neoplastic nodules and hepatocellular carcinomas in rats (Squires and
Levitt, 1975).
The biological nature and significance of neoplastic nodules in rodents
is currently a subject of controversy. Hirota and Williams (1979) found
11-153
that liver neoplastic nodules in rodents did not regress upon
discontinuation of the inducer carcinogen (fluorenylacetamide) , and new
nodules grew. However, no direct evidence was found for the
progression of the nodules to carcinomas. The Occupational Safety and
Health Administration (OSHA) , on the other hand, received testimony
from a large number of pathologists who urged the agency not to dif-
ferentiate between benign and malignant tumors when addressing
carcinogenic potential. Each of these pathologists cited a number of
carcinomas with benign (or apparently benign) precursors. Based on
this testimony, OSHA decided not to draw a distinction between benign
and malignant tumors in a carcinogenicity study unless that study could
demonstrate no evidence of progression to malignancy, according to a
set of criteria outlined by OSHA.
The National Cancer Institute (NCI) study has also come under question
because of a reexamination of this study by Melvin Reuber (1981), a
toxicologist at NCI. Based on his reexamination, Reuber concludes that
picloram is carcinogenic. Reuber reviewed the histological sections for
the rat and the mouse studies, and concluded that total neoplasms (both
benign and malignant) at all sites were increased for both male and
female rats in both the high and low dose treatment groups.
Carcinomas of the adrenal, thyroid, and pituitary glands were increased
in male and female rats, as were neoplasms of the liver and female
reproductive organs. In regard to mice, Reuber concludes that
neoplams of the spleen were increased in both male and female mice.
Reuber's findings of a significant increase in the number of neoplasms
at all sites in rats is partially a result of his comparing tumor inci-
dences in picloram-treated rats with pooled controls rather than matched
controls. NCI generally runs carcinogenicity tests for several chemicals
at the same time. Each study has a group of animals that are matched
(for age, sex, etc.) to animals in the treatment group. Reuber pooled
all the control animals from the various studies rather than comparing
the results for the smaller number of matched control rats. Although
this results in a firmer statistical basis for interpretation, it raises
questions regarding the effect of the differences in age, sex, and other
11-154
characteristics of control rats , along with the possible difference in
laboratory conditions and handling.
In another study, picloram caused proliferative lesions in endocrine
organs when picloram was administered in the diet at the maximally
tolerated dose and at half that amount. However, the author stated
that the increase in these lesions was small and inconsistent and not
indicative of carcinogenicity (Robens, 1978; abstract only). In a study
by Dow Chemical, U.S.A., rats were given dietary doses of 15, 50, and
150 mg/kg for 2 years. No increase in the incidence of tumors was
noted over control levels (Lynn, 1965; McCollister and Leng, 1969).
The data presented above do not allow a definitive statement regarding
the potential carcinogenicity of picloram. The histological slides from
the NCI study must be made available for further examination, and/or
another study with a firmer statistical foundation must be conducted.
Most reviewers of the NCI study, however, (EPA, for example) agree
with NCI's finding that picloram causes benign neoplastic nodules. It
seems advisable to adopt OSHA's position and suspect picloram as a
possible carcinogen until it can be shown that these nodules do not
progress to carcinomas.
Teratogenicity / Reproduction Limited data suggest that picloram does
not cause teratogenic or adverse reproductive effects. In a study by
Dow Chemical U.S.A., three generations of rats were given 3000 ppm
picloram in their diet. No adverse effects were noted with respect to
fertility, viability, gestation, body weight, lactation, or incidence of
terata. No data were provided. (McCollister and Leng, 1969) The
same study noted no effect on fertility or litter size when mice were
given a dietary dose of 1000 ppm picloram for 4 days prior and 14 days
subsequent to mating.
Thompson et al. (1972) found no terata or adverse effects on neonatal
development in rats given daily oral doses of 0, 500, 750, or 1000
mg/kg /day of picloram on days 6 to 15 of gestation. Maternal deaths
were noted at higher doses (5 at 750 mg/kg; 9 at 1000 mg/kg) between
11-155
days 7 and 17 of gestation. Mild diarrhea and hyperesthesia (excessive
sensitivity of the skin) were also noted at higher doses. At 500 mg/kg,
no overt signs of toxicity were noted. No effects on maternal weight
gain, litter size, pup weights, or number of implantations, corpora lutea,
and resorptions per dam were seen at any dose. Delivery and lactation
were normal, as were survival and development of the pups. When
fetuses were taken by Caesarean section on day 20, an increase in unossi-
fied fifth stemebrae was noted. However, this effect can be considered
transient, since weanlings delivered by normal births had fully ossified
sternebrae .
Mutagenicity As shown in Table 11-43, most tests show no mutagenic
activity of picloram.
Summciry An evaluation of important toxicity data is provided at the end
of this chapter.
3. MOBILITY AND PERSISTENCE
Fate in Soil
Picloram is generally considered to be relatively mobile in most soils
(TRW, 1981; Arthur D. Little, Inc., 1979; USDA, 1973). The mobility of
picloram can be attributed to its solubility (430 mg/1 for picloram; 40%
w/w for the potassium salt of picloram), to the low initial adsorption to
soil colloids, and to the slow breakdown of picloram by soil microorgan-
isms (NRCC, 1974).
In a review of leaching studies involving 24 soils from a number of agri-
cultural states and provinces of Canada, the National Research Council of
Canada (1974) stated that picloram penetrated to a depth of 30 cm or
more in 83% of the soils, to a depth of 60 cm or more in 58% of the soils,
and to a depth of 90 cm or more in 25% of the samples. (Application rates
ranged from 0.23 to 10.08 kg/ha). Helling (1971a) classified picloram as
"highly mobile" in a study of 40 pesticides. Phillips and Feltner (1972)
showed picloram to be highly mobile, using 3.36 kg/ha applied to a Kansas
sandy clay loam. After 3 years, the concentrations of picloram detected
were 229, 279, 278, 31, and 43 ppb in the 0-15, 15-30, 30-60, 60-75, and
75-120 cm layers of the soil, respectively. Bowes (1972) also found very
11-156
u
c
o
,^^
^
(U
t-H
•
^
(d
■«-»
nJ
V4
1— 1
■t->
O
«J
(U
Pu
>
0)
n)
(U
0)
(U
o
T)
2 Q
>.•
TJ
c
rt
o
• iH
c
B
o
I-l
s
00
00 oo o
r- r- <— I
ov cr> ^-'
I— I I— I
(U
(U
0)
(U
o
^
^
rt
«
(U
)h
u
Vi
^
a
ffj
0
(Nl
^^»
(M
r-
nD
t^
n^
^^^ y^ t^~
O^
1— 1
00 00 CT^
r^ r^ I— 1
QO ON N^
1— 1
«J
nJ
q; nJ oJ -g
<PQ
O
CO
a>
(U <U (D
U
<U Q) O
u u
d) (U
0)
U
U
O
U O H < U U H
n)
o
(0
u
<u
-o
<
<
O
U
I— I
(0
a
B
B
o
U
u
o
bO
B
o
o
00
0)
I— I
in
bO
O
O
in
CO
I
<
H
W
H
>-'
H
t— t
O
t— i
2
W
o
<
H
D
0)
I I
+ + +
I I I I
o
>
.1-1
>
a
(U
c
•»-»
•rH
CO
>>
(U
C
o
^
o
u
u
CO
(U
•4-»
H
u
CO
ver
tior
1— t
;3
13
C d "57
•i-t
tio
ssi
rn
cti O ^
-*-> U 0
3
:3 o C
•i-t
GO
= u u
u
+j +J +J
di
COO
D-
•^ ^-> -M
co
q^ 2 2
<
CO
O
I— I
O
u
13
o
o
CO
u
S
o
■«->
CM
0)
Sh
■*->
W
I— I
1—1
<u
C
o
a
I— I
a
m
CO
E
<
o
u
0)
bfi
c;J
o cu
o
CO T"
high mobility after applying 4.48 kg /ha picloram to a heavy clay and a
sandy loam in Saskatchewan. He found an average of 149, 55.5, 114.5,
128, and 30 ppb in the 0-15, 15-30, 30-60, 60-75, and 75-120 cm layers
of the soil.
The extent to which picloram moved in the soil was assessed along a
powerline right-of-way in the Pacific Northwest. Picloram moved down
to 30 cm, although most of it stayed above 15 cm (USDA, 1977). EPA
(no publication date provided [f]) states that picloram remains in the
upper 20-30 cm depth in most soils, except those of a sandy nature.
Norris et al. (1976a) found that when picloram was applied to a south-
ern Oregon hillside pasture, most of the herbicide remained in the
upper 6 inches (15.24 cm).
Because of its persistence, picloram can appear in soil leachate for a
considerable length of time (Arthur D. Little, Inc., 1979). Nine to 12
months after treatment, picloram was found at levels of 1 to 4 ppb in
leachate water (Arthur D. Little, Inc., 1979). In a study by Glass and
Edwards (1974), the first detection of picloram (1 ppb) at a depth of
240 cm was found one year after application. After two years, picloram
was still detectable at 0.5 ppb. Helling (1971b, c) found no correlation
between the mobility of picloram and the properties of 14 different soils
(e.g., pH, organic matter) due to the low adsorption of picloram in
these soils. Mobility of picloram was found to be correlated only with
the amount of water flowing through these soils.
TRW (1981), on the other hand, reviewed the literature and found that
adsorption (and thus mobility) is a function of pH, application rate, soil
type, and formulation, as well as water flux. Organic matter is consid-
ered the most important of these factors. Adsorption readily occurs in
soils contcdning a high organic content (Norris, 1970b) high concentra-
tions of humic acid (Khan, 1973), and significant amounts of the
hydrated oxides of aluminum and iron (Hamaker et al., 1963). Adsorp-
tion increases with increasing acidity, but is minimal in alkaline or
neutral soils (Youngson et al., 1967; Biggar and Cheung, 1973; Farmer
and Aochi, 1974; Grover, 1971; McCall et al., 1972). As would be
expected, given the various adsorption capacities of different soil
11-158
types, the movement of picloram is greatest in soils that are poor in
organic matter or in sandy, light-textured soils (Mullison, 1979; NRCC,
1974). The triisopropanolamine salt of picloram was found to be less
mobile than the potassium salt (Hunter and Stobbe, 1982). Bovey and
Scifres (1971) found that the leaching rates of esters and salts of
picloram were similar, and only the acid form was found below 5 cm.
Runoff studies have indicated that picloram is likely to move in water as
it flows over the soil (TRW, 1981; Arthur D. Little, Inc., 1979).
NRCC (1974) states, however, that runoff is likely to remove only small
quantities of picloram from the soil. Norris (1969) concludes that
picloram will be found in runoff when rainstorms are sufficiently intense
to cause overland flow rather than infiltration.
Norris (1969) found that when picloram was applied to three forest plots
in Oregon and Washington at rates of 0.5 to 1.0 lb /acres, the maximum
concentration detected in the runoff was 20-78 ppb. Bovey et al.
(1967) found that the potential for high concentrations of picloram in
the runoff increases as the time between the application and the first
rainfall decreases. Immediately after applying a 1:1 mixture of
triethylamine salt at the rate of 1:12 kg /ha on grassland watersheds,
heavy rainfall occurred, resulting in maximum concentrations in the
surface runoff of 400-800 ppb. Davidson and Chang (1979) found
similar results when picloram pellets were applied at a rate of 9.0 kg /ha
to 4.5% of a forested Arizona watershed. The maximum concentration
detected was 370 ppb, after a storm of 72 mm.
Other studies do not indicate such high concentrations of picloram in
the runoff. From a forest plot in Ontario, Canada, where picloram had
been - applied at a rate of of 0.9 kg /ha, the concentration in the
drainage was 38 ppb after 1 day, 26 ppb after 7 weeks, and 1 ppb
after 1 year. Baur et al. (1972) determined that 10-12 weeks after the
application of 1.12 kg /ha to 8 ha plots, about 10 ppb was found in
runoff water adjacent to the plots. Water sampled 1.2 km from the
plots after 8 days contained 1 ppb.
11-159
Conflicting results are documented for the effect of formulations in the
form of pellets and sprays. Bovey et. al. (1978) stated that the
potassium salt generated similar concentrations of picloram whether
applied as an aqueous spray or a pellet. A later study by Burnett and
Richardson (1980) showed considerable difference in the rate of runoff
loss for sprays and granules applied at 2 kg /ha to large watersheds in
Texas. They found a large initial concentration (112 ppb) immediately
after application of the spray, but not after application of the starch
xanthate granules (6 ppb immediately after application). Runoff loss
from the slow-release granules continued to increase for several weeks
while those from the sprayed watershed dropped to 0.1 ppb . Runoff
concentrations stayed at 20 ppb for 14 weeks, then dropped to 4 ppb
after 8 months. After 9 rainfall events, a total of 2.5% of the sprayed
picloram had been lost, while only 1.5% of the slow-release picloram had
been lost. Lower vertical mobility of the granules may also be indi-
cated, since picloram concentrations in the upper 15 cm of soil were
greater for the granules than for the spray.
Picloram is well-documented as being moderately to highly persistent,
with half-lives of 1 to 13 or more months (Mitchell, 1969; Schlapfer,
1977; EPA registration files, no date; Goring et al. , 1965; Altom and
Stritzke, 1973; Hamaker et al. , 1967.
The persistence of picloram is a function of soil type, moisture, and
temperature. It is very persistent in cold, dry climates, and in clay
and sandy loam soils having a low percentage of organic matter. (Caro
et al. , 1974; Merkle et al. , 1967; Hunter and Stobbe, 1972; Herr et
al. , 1966b), Additionally, dissipation is very slow under conditions of
low soil moisture (Hunter and Stobbe, 1972) and high pH (Youngson et
al. , 1967). The effect of organic matter is unclear (Arthur D. Little,
Inc., 1979). Barnside et al. (1971) and Herr et al. (1966) state that
persistence increases with organic matter, while Helling (1971a, b,c) and
Merkle et al. (1973) state that it decreases with organic matter,
Picloram does not serve as a good energy source for microorganisms,
although it is cometabolized with other energy sources, and amounts
degraded may be small, even under the most favorable conditions.
11-160
The mechanism of microbial degradation is unknown, and it may vary
from organism to organism. It is believed, however, to be a
decarboxylation and ring cleavage (TRW, 1981). Merkle, et al. (1974)
used lab studies to show that the ring-labeled picloram is degraded to
produce CO„ at approximately the same rate at which the carboxyl-
labeled carbon reacts. The by-products identified were 4-amino-2,3,4-
trichloropyridine and 6-hydroxy-3,5-dichloro-4-aminopiclonic acid.
Residues and Persistence in Water
Initial picloram residues in water have been shown to be highly
variable. Residual concentrations decrease rapidly, however, and
picloram appears to be less persistent in water than in soil. The
routes of loss of picloram from water are unclear.
USDOE (1980) documents two studies (giving no primary sources) in
which picloram was applied aerially at a rate of 1 lb /acre to
transmission line rights-of-ways. In the first study, involving a
segment in the Cascade Range in Oregon, residual concentrations
peaked at 15 ppb 30 minutes after application to a site approximately
350 feet from the stream sampling area. After 1 hour, the concen-
tration was below the detection level of 3 ppb, and picloram was not
detected in the subsequent 5-month period. In the same study, also at
1 lb /acre, no residues were detected (limit, 2 ppb) for 9 months after
application, although equipment failure resulted in no monitoring in the
first 48 hours. It was found later that direct application to the stream
had occurred. During the 9 months, 70 inches of precipitation had
fallen in this area on the Oregon coast, so it is likely that picloram
residues were rapidly diluted and flushed from the area.
Similar results have been found in other stream studies. Five months
after 1 kg /ha picloram was applied to plots located near the head of a
small stream, Haas et al. (1971) found no detectable picloram at
distances of 0, 0.8, and 1.6 km from the plots, even though runoff
water contained a maximum of 29 ppb during that time. In another
study in which runoff water entering a creek contained 13 ppb
11-161
picloram, concentrations in the creek were 0.4 ppb or less (no time
given) (Baur et al. , 1972).
Standing water may contain higher concentrations of picloram. Haas et
al. (1971) applied picloram directly to a livestock pond at a rate of 1.12
kg/ha and found an initial concentration of 500 ppb, which dropped to
about 5 ppb after 100 days and remained at that level for another 100
days. Picloram was not detectable (limit, 1 ppb) 1 year later. In the
same study, a more complicated system was examined in which one large
pond received picloram from direct application (at 1.12 kg /ha) and from
runoff from surrounding grassland. The initial concentration in this
pond was as high as 1000 ppb immediately after application. After a
heavy rainfall this pond overflowed into 2 smaller ponds, which were
found to contain 10 to 20 ppb immediately after overflow occurred.
After 100 days, however, concentrations in all ponds decreased to 1 to
2 ppb. The author found from both of these studies that the loss of
picloram was concentration-dependent, with an initial rate of loss of 14%
to 18% per day in the first 100 days, and a subsequent rate of loss of
1% per day in the next 100 days.
Picloram is not subject to significant microbial or chemical degradation
in water; photodegradation is considered the major degradation route
(NRCC, 1974; TRW, 1984). However, photodegradation is usually
significant only in the upper surface layers of water. This is demon-
strated by the photolysis half-lives of picloram, which range from 5
days in 1-inch deep containers to 60 days in 12-foot deep non-
circulating containers. (Hedelund and Youngson, 1972). Thus,
primary routes of loss remain unclear.
Indicators of Potential Ground Water Contamination
Table 11-44 provides information on parameters associated with the
mobility of picloram. These parameters, and their associated thres-
holds, have been suggested by EPA for use in assessing the potential
for pesticide contamination of ground water. A discussion of these
parameters and thresholds, and the methods for arriving at designated
values for individual herbicides, is presented in the main body of the
11-162
report as part of the discussion of the fate of herbicides in the
environment .
TABLE 11-44
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
PICLORAM
Indicator
Solubility
K
oc
Speciation at pH 5
Hydrolysis half-life
Photolysis half-life
Vapor pressure
Value for Picloram
Threshold
430 ppm at 25''C
(potassium salt:
highly soluble)
>30 ppm
13
<300-500
Anionic
Anionic
(negatively charged)
Stable
>6 months
<1 week
6.16 X lo'^
Hg at 20OC
mm
>3 days
<10 mm Hg
* ND = no data.
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Kenaga (1969), Mullison (1972), Bovey and Scifres (1971), and others
concluded that picloram had low toxicity to birds. Kenaga (1969)
studied the effects of picloram on three generations of Japanese quail
by supplying 1000 ppm to their feed. The author concluded that there
was no effect on mortality, egg production, or fertility. The author
also determined the LC--. for bobwhite quail and mallard ducks to be
23,000 and 385,000 ppm, respectively. Norris (1976) reported an LD-.
for birds to be greater than 2000 mg/kg, and the author noted that
1000 mg/kg produced no effect. Tucker and Crabtree (1970) reported
11-163
o
in
CQ
<
Q
Pi
I— i
CQ
O
H
<
Pi
O
u
l-H
fa
o
>^
H
o
X
o
o
to
c
0)
B
e
o
o
o
•i-i
I— I
B
o
fa
o
<0
u
I— 1
(NJ
in
■»->
,,»i^
C^
l-H
,Q
in
*
O^
**-'
flj
r-
r— 4
(—1
^
o^
nJ
'-^
•k
O
1— <
-"^v
•
x^
v_^
■«->
<T>
•«
o^
^3
<u
nO
•
vD
*
cr>
l-H
4^
O
C
•
^
1— 1
(T)
0)
l-H
nJ
^
1— t
-*->
rt
""^
^
^
0)
»-H
—
^-^
$H
(U
rt
l-H
• IH
rt
■♦-»
0)
OC
bO
X
bO
o
I— H
TJ
C
ci
T3
C
:3
• i-i
c
0)
(U
(U
H
K
nJ
fcii!
32
^
■«->
l-H
Oi
o
c
T3
o
-0
bo
a
u
•^
o
3
0)
!h
^
C
en
0)
O
■4-'
O
«k
o
C5
E
o
bO
o
MH
• iH
-t-»
o
13
-t->
•iH
l-H
cu
X
E
130
(30
B
E
bO
bO
E
bO
bO
E
bO
E
o
o
E
a
E
cu
cu
bO
E
3
O
CU
bO
■)->
u
o
E
73
1
73
sO
o
o
o
• IH
l-H
bO
>.
l-H
'^
o
o
o
O
CO
•k
o
o
CU
D
vD
o
o
o
o
;h
CO
o
o
o
bO
^
1— H
o
A
o
A
o
in
A
o
o
o
II
l-H
II
in
A
in
A
bO
o
>>
•»H
O
>+H
-t->
1
l-H
>-H
o
o
o
l-H
1
73
o
o
o
o
E
• IH
• iH
^
^
in
in
in
1
in
in
in
in
o
■4-»
o
bO
Q
Q
O
o
o
U
O
O
U
o
o
HH
V4H
MH
• iH
J
J
J
in
in
J
J
-J
J
l-H
(U
-C
^
a
C
C
C
0)
<u
0)
(U
l-H
l-H
l-H
l-H
fc4
nJ
nS
CEl
rt
>
>
>
>
CM
• iH
• IH
3
• IH
3
C!
<u
:3
C
0
U
>
cr
cr
cr
>
>
cr
•iH
a;
(U
(U
•fH
• iH
0)
bo
bO
bO
73
13
13
Xi
•4->
• IH
<|H
• IH
4->
-M
• fH
O
o
u
o
o
O
O
o
H
2
<
<
<
2
2
<
M
u
3
T3
M
T)
0)
• IH
o
(U
l-H
l-H
a
a
in
2
cr
■ IH
o
PQ
CO
u
• IH
cr
• IH
cr
.|H CO
0)
• IH
en
tn
^ 73
4:
(U
0)
Bobw
5-7
C
a
OS
1-2
o
u
o
9)
CM
o
C^
r-
O^
a^
l—i
r-l
X
(U
0)
■4-»
X
^
rt
TJ
^
c
u
nJ
'O
»^>»
c
un
m
t^
o^
^
(— 1
(U
^"^
^
o
3
X
H
w
Q
Pi
hH
Q
CQ
ID
2
O
H
1— 1
H
O
o
2
<
O
o
LO
I— 1
a*
1
t— 1
fa
o
w
J
>•
CQ
H
<
1— 1
O
1— 1
X
o
H
CO
+->
C
(U
8
a
o
U
;3
o
a
X
a;
>^
I
^4
O
e
o
o
o
0)
1— 1
o
>
•1-4
3
(tJ
cr
3
(U
s
-o
u
•rH
o
O
fa
<
o ,il
bo
bO
o
C
Xi
u
O
o
^ bo
T3
u
(0
U
•1-1 ^
^3
O
bO
bO
fa
u
Ou 73
u
o
E
OS
u
+J
bO
bO
(U
in
^4
0)
73
C
O
o
(U
(A
■»->
o
c
•4->
(U
^4
O
■*->
ni
X
c
(1)
E
u
E
U
o
a;
>
•i-t
bO
bO
bO
E
o
o
o
(3
o
o
in
o
o
I-H
>
cr
a;
<
-a
■«->
c
o
• l-H
■*->
ni
0)
C
<u
bO
I
en
(U
>
•i-t
u
73
O
u
a,
d)
u
I
c
bfi
fa
CO
(U
o
(NJ
0)
c
o
U
C
(U
bO
I
I
^. "J
q; o
bo C
bO
fa w
« o
2
CO
(U
CM
T3
CO
(U
C d)
O MH
•1-1
si ••-'
I -
O
a
bo
bO
I
CO
CO
o
u
'^ 5
o :;3
•PH
o o
.1-1 .rH
■4-> •4->
o o
1
a
E
>^
CO
di
CO
)^
>
73
nJ
O
2
bO
■•-»
bO
(U
o
01
E
u
o
73
<u
C cu
XI
o
CJ CO
> E
E
bO
bO
E
o o
o o
o o
in cvj
A A
o o
un in
U O
c
•
• 1-4
a;
•
>
CD
• IH
bO
o\o
in
•♦->
0
0
2
0^
w
ns
CO
(U
C
^ «J
(0
M
0
.pH
A
ix:
1—1
u
• rH
3
T3
1— t
cr
0
<0
>■
CO
(D
(U
T3
c
«j
r-
a
1
rt
in
•-0
C
C
nt
rt
(0
CO
ni
rt
0)
(U
^
^
^
p^
an LDcn value for mallards and pheasants to greater than 2000 mg/kg.
Heath et al. (1972) and Hill et al. (1975) reported LC values for
Japanese and bobwhite quail, ring-necked pheasants, and mallard ducks
to be greater than 5000 ppm. These data are summarized in Table
11-45.
Fish
The toxicity of picloram is shown in Table 11-46. Arthur D. Little,
Inc. (1979) concluded that picloram was toxic to fish, based on the fact
that 96-hr LCj.- values ranged from 1.55 to 26.0 ppm, depending on the
species of fish and the formulation of picloram. A review by the USD A
(1973) stated that the isooctyl ester would be toxic to sensitive species.
TRW (1981), on the other hand, stated that picloram and its salts were
low in toxicity to fish, based on data provided by EPA (publication date
not provided [f]), and Sargent et al. (1971). Data they cited was
primarily from 24-hr toxicity tests, which may explain the difference
between the TRW and Arthur D. Little, Inc., conclusions.
Kenaga (1969) stated that a field application of 3 lb /acre of picloram
was not likely to result in contamination greater than 1 ppm, due to
dilution, adsorption, and degradation.
A study by Woodward (1979) concluded that picloram reduced growth in
cutthroat fry at concentrations above 0.61 ppm, and increased fry
mortality at concentrations greater than 1.3 ppm. No adverse effects
were noted at concentrations below 0.290 ppm. Lorz (1979) reported
the effects of picloram on Coho salmon. In salt water, 0.29-19.8 ppm
for 144 hrs produced little effect, but 0.29-.62 ppm produced an
®
unexplained mortality of 75%. The effect of Tordon 101 at 1.35 and
1.8 ppm had little or no effect on seaward migration of the Coho
salmon.
Lower Aquatic Organisms
Hardy (1966) studied the effect of 1 ppm of the potassium salt of
picloram on a food chain of algae, daphnids, and fish. The author
found that the algal growth was not retarded, and that the daphnids
and fish appeared to behave and reproduce normally. Table 11-47 sum -
11-166
(U
u
u
o
w
in
^-s
t^
OJ
o^
r-
r-t
o^
^•^
1-1
^-^
g
0)
:3
£
bO
{3
*■"*
rt
x--<.
ni
h
a
w
vO
t^
rH
1— 1
T3
^^
73
^-^
'O =
c =
u
CO
13
(U
u
O
bo
rt
O
O
I— <
0)
^
fe
<
!^
I
<
w
fa
O
H
<
Pi
O
u
PL,
fa
o
H
I— I
O
I— (
X
o
e
3
(A
H
en
(U
•i-i
o
0)
o
•
00
I
in
CO
in
I
in
in
en
o
o
in
o
o
CO
in
•
nO
I— 1
CT^
f-t
ra
sO
l—^
vD
"^
vO
1
1
<M
1— 1
CO
in
o
O
o
■«J*
"^
(M
(M
<N3
1
1
O
(\3
O
O
O
■«^
in
CO
"^
i-H
oa
CM
O^
(M
o
u
3
O
3
;3
o
o
■4^
u
u
:i
4->
-t->
o
u
^
^
-*-»
o
o
Xi
^
(U
c
c.
M
•ri
'n.
rt
a
nJ
J
^
^
nS
A
U
o
S
o
■M
o
Xi
(0
,£3
CO yil
3
r— I
nJ
O
o
c
- '2
bO 0)
I— I oj
CQ fa
^ in no
• • ff
CO o o
■^ c^ c^
E
E
O
in
1
J
J
U
^
"•
^
^
^'
^
^
^
"*
""
^
^
^
*^
^'
""
^
^
H
H
hJ
h
)h
u
u
u
u
u
u
U
u
u
u
u
u
u
u
u
u
u
u
U
A
1
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
1
A
A
X,
1
1
1
00
1
1
oo
1
1
1
1
1
1
00
1
1
1
1
1
1
1
■^
^
•^
o^
O
"^
o^
'^
(M
CM
<V1
fM
rg
^
CO
00
CM
CM
<Na
CM
CM
CM
(M
(M
•M
■♦->
A
en
T3
•«->
■J-"
A
CO
13
3
3
13
cfl
O
O
."^
•+J
•4->
C
0
0
■*-»
U
u
M-t
UJ
ri
J3
O
u
Jh
(4
+->
4-»
U
o
o
P-H
E
l-H
-»->
■M
y
^
^
13
en
u
4->
-t->
:3
^
^
1— 1
4)
^
0
o
A
C
0
0
o
o
CTJ
1— 1
cn
en
cn
o
A
o
A
0
A
•r3
(4
(0
nJ
(ti
h
u
^M
nJ
o
OJ
cti
4J
0
p:5p:iOCQCQeQfQOPi
Cri 0 O
(4
-»-»
*■*
-♦-»
-t-»
l-H
1— (
l-H
h
(tJ
t^
ceJ
H
c
00
W
U1
en
en
cn
CO
0
CM
(M
l-H
CM
(M
E
E
E
E
(TJ
CJ
:i
:3
3
13
.1-1
c
c
• rH
.f-i
• IH
• IH
9
c
0
0
en
CO
en
CO
s
A
o
-0
T3
cn
cn
CO
CTJ
CO
T3
u
v*
V4
-*->
■4->
+->
-<->
• iH
o
(U
0
o
o
o
o
o
o
■X4
H
H
H
fa
fa
fa
fa
<
(U
•IH
E
l-H
o
fa
O
fa
o
J^ cn
H
en
<o
13
• iH
E
l-H
A
H
I
<
CO
CO
<
O
Pi
O
U
l-H
H
<
D
a
o
o
H
<
O
O
>^
H
H-l
o
n
X
o
0)
u
o
CO
en
■♦-»
0)
E
a
o
O
o
(U
a
CO
c
o
•♦-»
I— t
e
u
o
fa
»4
0)
I— I
PQ
00
0«'
a
o
O
c
(0
CO
sO
CO
CO
0)
(0
o
C
rt
o
J E
dp
0
C
0
***^
^
TJ
-0
• «»
• rH
ced 8.
ity
0
G
T3
U
0)
'0
0
0)
0
2
^ i
Mh
(UdP
^ E
odu
ctivi
:3
0
.IH
>
1
e
E
a
0 in
C 0-
u 5
i-H
(U
r
•IH
^1
0
0
u
l-H
>
• |H
>
u
-0 13
0) 0)
y 0
3 3
0
CO
<u <u
3 3
u a
u
0
sD
00
no 'O
II
II
73 'O
;3 ^
3
^
0^
^
^
3
P ?
? ?
en C
(fl
&i
(0
(0
u u
0
0
^i^ >H
o •'^
0
^
u
a a
in
in
a a
P4 0}
a c
^
C
^
c
u
U
X w
X
0
MH
0
Mh
0
e 6
J
J
E E
(U n)
v
8
B
a &.
a cu
V4 U
V4
u
<4H
•4^
U
^H
0
0)
Mh
a cu
u
a a
-^ S^
^
a
a
0 0
1
1
0 0
' iJ
1
^H
MH
MH
00 en
'St*
00
00 CO
rt< 73
"^
(U
r-H
9)
i-i
(U
CO in
(M
-"i^
CO in
X
^
•F"
•^
s
B
(0
c
a
cu
^
0
0
E
CO
c
C
^
X)
(4
l-H
(4
l-H
00
(0
>^
0
ns
a
0
4->
u
(0
0
■4->
• IH
• |H
>>
>>
(fl
0
l-H
r-H
S
a
Si
X
>^
»H
0
0)
cu
Oa
0
PQ
2
CO
<
Q
W
(M
(\>
(NJ
l-H
1-1
1—1
(NJ
0
0
0
13
Tl
'O
T3
<M
r-H
l-H
l-H
(U
0)
(U
(U
■»-*
-4->
■♦J
+->
0
0
0
13
0
13
CO
•4->
CO
CCJ
■*->
CO
CO
}h
»H
»4
»4
■M
•*-»
•*-»
'4->
0
0
0
0
0
0
0
0
H
H
H
H
2
z
2
2
00
13
(D
■4-»
• iH
y
C
0
• IH
■4-»
•
u
1
-«->
*
c
<NJ
(1)
c
0
CO
13
0
3
I-H
0
CJ
C
rg
marizes the data on the effect of picloram on lower aquatic organisms.
Livestock
MuUison (1979), EPA (publication date not provided [f]), NRCC (1974),
Norris (1976), and others stated that picloram had a low toxicity to
warm-blooded animcds. Williams (1971b) fed 23 mg/kg/day to cattle, and
100 mg/kg/day to sheep for 1 month and observed no adverse effects.
Lynn (1965) reported^ that sheep showed no adverse effects when fed
the potassium salt formulation (25% active ingredient) at a rate of 4650
mg/kg, but the Tordon 101 formulation produced toxic effects and
subsequent death in 3 days at 2530 mg/kg. Cattle appear to be a bit
more sensitive, with 1900 mg/kg representing the toxic dose. It should
be noted that the doses used in this study are very large in comparison
with those that could result from exposure. Mullison (1979) reported
LD^rt values of 6000 mg/kg for chicks, greater than 1000 mg/kg for
bO
sheep, and greater than 750 mg/kg for cattle.
Bees
Johansen (1980) and the University of California (1975) reported that
picloram showed a low toxicity to bees. Johansen (1980) reported the
LD^- values for both picloram and Tordon (formulation not given) to be
15 ug/bee. Morton et al. (1972) found that newly emerged honeybees
fed concentrations of 0, 10, 100, and 1000 ppm by weight in 60% su-
crose showed no reduction in half-life. The authors actually reported
an increase in half-life of bees fed 100 and 1000 ppm. Moffett et al.
(1972) concluded that Tordon 22K and Tordon 212 applied at a rate of
4 lb a. i. /acre were non-toxic to bees confined in a 20 gal/acre water
carrier.
Soil Microorganisms
The EPA (publication date not provided [f]), Mullison (1979), and
NRCC (1974) stated that picloram was low in toxicity to soil micro-
organisms. Goring (1971) noted that it was broken down in soil and by
pure cultures of a variety of microorganisms. In another study, Goring
11-169
et al. (1967) subjected 46 different common microorganisms to concen-
trations of between 0 and 1000 ppm, and found that it did not retard
growth or development of any of them except Thiobacillus thiooxidans,
which was inhibited at 1000 ppm but not at 100 ppm. The authors also
concluded that rates of carbon dioxide evolution and urea hydrolysis
were unaffected. At 1000 ppm nitrification of ammonium ions to nitrite
ions was partially inhibited, but not at 100 ppm. Tu and Bollen (1969)
found little effect up to 1000 ppm on ammonification , nitrification, sulfur
oxidation, and organic decomposition.
Arnold et al. (1966) found that growth of Aspergillus niger was not
depressed by the addition of 0.4-5.0 ppm picloram in nutrient solution,
although it did accumulate in the mycelia. A study by Hameed and Foy
(1974) assessed the effect of 1 to 1000 ppm picloram on five species of
soil fungi (Trichoderma viride, Fusarium oxysporum, Helminthosporium
victoriae, Penicillium lanosum, and Aspergillus flaves) . All species
grew, but were not able to utilize picloram as a sole source of carbon
and nitrogen.
Hardy (1966) and Elder et al. (1970) investigated the effect of
picloram on algae. The first study found that 1 ppm picloram in water
had no effect on algae, and the second study found that picloram had a
low toxicity to many fresh water and marine algae species at
concentrations approaching its maximum solubility in water.
Bioaccumulation
A number of studies have shown that picloram does not bioaccumulate in
animals. When steer were fed 200-1600 ppm picloram, a maximum of 0.3
ppm was found in muscle and fat, and up to 18 ppm in kidneys. The
concentration fell to less than 0.1 ppm within 3 days of withdrawing the
picloram from the diet (NRCC, 1974). McCollister and Lang (1969) and
Norris (1971) stated that cattle and other mammals eliminated 98% of
ingested picloram as an unchanged compound in the urine. The EPA
(publication date not provided [f]), and Hardy (1966) found that
picloram did not accumulate in aquatic food webs or chains.
11-170
Studies by Arnold et al. (1966) and Hameed and Foy (1974) did indicate
that picloram was accumulated in the mycelia of a variety of fungal
species .
Toxicity Data Evaluation
The evaluation of carcinogenicity data for picloram has been stated on
the previous page: The data do not allow a definitive statement.
Insufficient data are available to indicate with any certainty that pic-
loram does not cause teratogenic effects. Although most of the tests on
mutagenicity show no effect, an insufficient number of reliable tests
have been conducted to draw a definitive conclusion.
Dow Chemical U.S.A. has replaced all studies conducted by IBT on
picloram I namely a teratogenicity test using the mouse, a skin-patch
test using humans, and two chronic oral studies using the dog and the
rat. Two teratology studies and one chronic study done by other
laboratories already existed in EPA files.
A registration standard on picloram is currently being prepared by
EPA. Data gaps to be filled will be identified in that document.
11-171
M. TEBUTHIURON
1. INTRODUCTION
Tebuthiuron is the common name for a substituted urea herbicide,
1- ( 5-tert . -butyl-1 , 3 , 4-thiadiazol-2-41) -1 , 3-dimethylurea , manufactured
by Elanco Products Company, a Division of Eli Lilly and Company. It
is also called Graslan , Brulan , Tiurolan , EL-103 , Preflan ,
/8\ /Bv (B\ (S\
Perfmide , Tebulan , Prefmid , and Spike . Its chemical structure is
shown below.
{CH3)3C
N-C-NHCK
II
0
Relevant physical and chemical characteristics are presented below in
the discussion of tebuthiuron in soil.
2. TOXICITY
Acute Toxicity
Tebuthiuron shows moderate toxicity in acute tests. Lilly Research
Laboratories (1982) states that the acute oral LDj.^. values are for the
rat, mouse, and rabbit are 579 mg/kg, 644 mg/kg, and 286 mg/kg ,
respectively. This study also reports that rabbit tests showed no
dermal irritation and only "slight transient" eye irritation. An infor-
mation sheet by Elanco Products Company (1980) states that when rats
were given a single oral dose of 500 mg Spike SOW per kg of body
weight, no effects were observed for a period of 14 days after
treatment.
11-172
Mammalian Metabolism
Tebuthiuron appears to be rapidly eliminated. More than 85% of labeled
tebuthiuron (single oral dose) was excreted in 96 hours in the rat,
rabbit, mouse, dog, duck, and steer. (Lilly Research Laboratories,
1982).
Special Studies
The only available literature on the chronic toxicity of tebuthiuron is from
®
a siimmary of information about Graslan provided by Lilly Research
Laboratories (1982). This report states that two multi-generation studies
have shown no evidence of carcinogenicity, mutagenicity, teratogenicity,
or impairment of reproductive performance. In a two- generation rat
study, a minimal depression in bodyweight gain was observed in one sex,
in one generation of rats at levels of 200 and 400 ppm. The no-effect
level was found to be 100 ppm or 7 mg/kg/day tebuthiuron. Based on
these studies, an acceptable daily intake was determined to be 0.0737
mg/kg/day tebuthiuron. Total maximum dietary intake was determined to
be 0,0128 mg/kg/day, using established tolerances as a basis for intake
levels.
Summary An evaluation of important toxicity data is provided at the end
of this chapter.
3. MOBILITY AND PERSISTENCE
Fate in Soil and Water
Tebuthiuron appears to be a mobile and persistent herbicide. Manufac-
®
turer's information provided for Graslan states that "GRASLAN pellets,
deposited on the soil surface, are disintegrated by the first significant
rainfall and the herbicide is moved into the soil. Subsequent rainfedl
moves the herbicide into the root zone where it is absorbed by the roots
of woody plants. . . . The relatively long soil half-life and some vertical
movement are considered necessary for the proposed use. ..." Lilly
Research Laboratories (1982) reports that tebuthiuron moved to a depth
of 46-61 cm in one study, although other studies showed no tebuthiuron
below 46 cm. In a study by Reed (1982), tebuthiuron moved to a depth
11-173
of 26 cm after 6 weeks in a silty clay, and to a depth of 30 cm (maximum
depth sampled) after 6 weeks in a sandy loam and a sandy loam with high
organic matter content. Baur (1978) found that 20 cm of rain distributed
tebuthiuron throughout a 20 cm soil profile in both a clay loam and a
sandy loam. In a soil thin-layer chromatography test, tebuthiuron was
found to move with the water front in a sandy soil, although less move-
ment was found in a loam and a silt loam (Chang and Stritzke, 1977).
Different results were found by C. D. Christensen et al. (1974), who
found "little vertical movement" and "essentially no lateral movement"
when tebuthiuron was applied along several miles of highway and railroad
right-of-way in Massachusetts, New York, Pennsylvania, and Kentucky —
even along slopes up to 20%. No further information was provided in a
review of this study by Reed (1982).
Lilly Research Laboratories (1982) reports that wells in or adjacent to
®
Graslan -treated areas have contained no residues of tebuthiuron.
Contradictory information is avedlable on the potential for movement via
runoff. Bovey et al. (1978a) found up to 22 ppm in runoff when rainfall
occurred shortly after application. Lilly Research Laboratories (1982)
reports that no detectable residues were found in runoff water from an
Arizona watershed, and a maximum of 0.18 mg/1 was found in a catchment
basin in a watershed in Texas. The maximum level was found after 7.1
inches fell in one day.
Tebuthiuron appears to be very persistent, with a half-life of 12 to 15
months in areas with 40 to 60 inches of rainfall (Thomson, 1975). Lilly
Research Laboratories (1982) found second and third half-life values to be
approximately 125 and 525 days, respectively, in areas with more than 30
inches of rainfall. Two studies found that tebuthiuron "may persist more
than a year" (C. D. Christensen et al. , 1974; Klingman and Ashton,
1975) (no further information provided) . Precautions on the label (Elanco
Products Co., 1980) include the statement that its "presence in the soil
may prevent growth of other desirable vegetation for some years to
come . "
11-174
Degradation appears to be a microbial process, including ring cleavage
to form volatile products, and demethylation of the urea moiety (Lilly
Research Laboratories, 1982).
No information was found on residues or the persistence of tebuthiuron
in surface waters.
Indicators of Potential Ground Water Contamination
Table 11-48 provides information on parameters associated with the
mobility of tebuthiuron. These parameters, and their associated thres-
holds, have been suggested by EPA for use in assessing the potential
for pesticide contamination of ground water. A discussion of these
parameters and thresholds, and the methods for arriving at designated
values for individual herbicides, is presented in the main body of the
report as part of the discussion of the fate of herbicides in the
environment.
TABLE 11-48
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
TEBUTHIURON
Indicator
Value for Tebuthiuron
2300 ppm at 25°C
Threshold
Solubility
>30 ppm
K
oc
620
<300-500
Speciation at pH 5
Catonic
(positively charged)
Anionic
(negatively charged)
Hydrolysis half-life
ND*
>6 months
Photolysis half-life
stable in light
>3 days
Vapor pressure
non-volatile
<10 mm Hg
* ND = no data.
11-175
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Insufficient information is available to evaluate the effect of tebuthiuron
on birds. Low toxicity is suggested by a chronic one-generation repro-
duction study in which 100 ppm tebuthiuron caused no toxic symptoms
in bob white quail, or mallards (Lilly Research Laboratories, 1982).
Fish and Lower Aquatic Organisms
Limited information suggests that tebuthiuron is not toxic to fish and
lower aquatic organisms . A report by Lilly Research Laboratories
(1982) found that the LCr^ or EC(.^ for Daphnia magna, eastern oys-
ters, pink shrimp, fiddler crabs, bluegill, and rainbow trout ranged
from 48 mg/1 to 320 mg/1. No symptoms of toxicity were observed in
chronic embryo larvae studies with these organisms when exposed to 9.3
mg/1 tebuthiuron. Thomson (1975) states that tebuthiuron is low in
toxicity to fish.
Bees
Tebuthiuron appears to be non-toxic to bees. No greater mortality of
honeybees was observed after they were sprayed with 30 g/1 tebuthiu-
ron than after they were sprayed with water (Lilly Research Labora-
tories, 1982).
Livestock
Tebuthiuron appears to be non-toxic to livestock. After being fed 10,
30, and 100 ppm tebuthiuron for 162 days, no toxic symptoms were
noted, and weight gain was normsil except for a slight reduction at the
®
highest dose. In another study, Herford cows in Graslan -treated
pastures gained 108 lb /head, as compared to 44 lb /head in untreated
pastures (Lilly Research Laboratories, 1982).
Toxicity Data Evaluation
More publicly available information is needed on tebuthiuron. However,
since it was registered after the 1972 data requirements were in place,
it can be assumed that the manufacturer conducted the complement of
tests required by EPA at that time, and that the results were found to
be acceptable by EPA. No tests were conducted by IBT.
11-176
N. TRICLOPYR
1. INTRODUCTION
Triclopyr is the common name for the herbicide ( (SjSjS-trichloro-Z-
pyridyUoxy) acetic acid, produced by Dow Chemical U.S.A. Triclopyr
is available in two formulations: Garlon 3 A , a triethylamine (TEA) salt
®
that is water-soluble and contains methonol, and Garlon 4 , an ethylene
glycol butyl ether ester (EGBE) that is oil-soluble and water-emulsifi-
able (TRW, 1981). DOWCO 233 is an early name used to refer to tri-
clopyr formulations (Thomson, 1975); however, no information is
available on its properties. Garlon 3 A contains 3 lb triclopyr acid
®
equivalent per gallon and Garlon 4 contains 4 lb triclopyr acid equiv-
alent per gallon. Triclopyr is a picolinic acid derivative with the
following structure:
Cl^^ ^0-CK-C
^
N
\
OH
Relevant physical and chemical properties are presented below in the
discussion of the fate of triclopyr in soil and water.
2. TOXICITY
Acute Toxicity
Available information suggests that triclopyr can be considered slightly
®
toxic, while Garlon formulations have low toxicity. LD-n values range
from 713 mg/kg for triclopyr (the active ingredient of Garlon) to 2830
®
mg/kg for Garlon 3A (see Table 11-49). The acute dermal LD-^ in
rats is greater than 4000 mg/kg, although repeated prolonged contact
may cause irritation. An inhalation study showed that 100% of the test
®
rats survived a 1-hour exposure to 3-20 dilutions of Garlon 3 A in air.
11-177
Transitory nasal irritation to rats was noted after a 4-hour exposure to
.®
Garlon 4 aerosol (Dow Chemical U.S.A.; 1981a).
While Garlon 4 is essentially non-irritating to eyes, Garlon 3 A can
cause serious eye injury in humans. Permanent impairment of vision
can result from exposure. Effects include severe conjuctival irritation,
moderate internal redness, and moderate to severe corneal injury, which
(tests show) is not healed after 21 days. Washing is not effective in
preventing these effects (Dow Chemical U.S.A.; 1981a).
Special Studies
TRW (1981) cites the following information by Dow Chemical U.S.A.
Triclopyr, administered at 30 mg/kg/day, was not carcinogenic in rats
and mice. In dominant lethal and in host-mediated assays, triclopyr
was not mutagenic. At 200 mg/kg/day, it exhibits a reproductive
toxicity effect and is considered mildly fetotoxic.
Only one publicly available study was located. Moriya et al. (1983)
found no evidence of mutagenicity in an Ames / Salmonella test system
and an Escherichia coli WP2 test system.
Summary An evaluation of important toxicity data is provided at the
end of this chapter.
TABLE 11-49
ACUTE ORAL TOXICITY OF TRICLOPYR
LD^Q (mg/kg body weight)
Rats Guinea
Rabbit Pig Source
Form
Male
Female
Triclopyr,
technical
grade
*
713
Triclopyr
729
630
Garlon 3 A
2830
2140
Garlon 4
2460
2140
Thomson (1976)
550 310 Dow Chem. U.S.A.
(1979, 1981)
* Unspecified sex.
11-178
3. MOBILITY AND PERSISTENCE
Fate in Soil
TRW (1981) states that triclopyr is considered a mobile herbicide, citing
a review by EPA of registration file material. Manufacturer's
information states that triclopyr does not readily adsorb to soil particles
(Dow Chemical U.S.A. 1981). The mobility of triclopyr was studied by
Hamaker (1977a) using a loam sand that was low in organic matter
(0.62% organic carbon). Water was applied at a rate of 0.5 inches /day
for 45 days. The results indicated that 75% to 80% of the triclopyr
passed through a 12-inch column of soil between days 11 and 15. A
degradation product, trichloropyridinol , was less mobile, requiring 13
inches of applied water to move through the column, as compared to 7.5
inches for the parent compound. McKellar (1977) studied the leaching
potential in six soils (ranging from clays to loamy sands) under field
®
conditions in six states. Garlon 3 A was applied at a rate of 3
gal/ acre, and the rainfall was said to be normal, although the rates are
not given. Small amounts (concentrations not given) of triclopyr and
its degradation products were found at depths of 6 inches to 18 inches
after 28 to 56 days. McKellar (1977) notes that the degradate
trichloropyridinol is less mobile than triclopyr.
A somewhat confusing picture is presented in studies by Hamaker
(1975) in his determination of distribution coefficients for the TEA salt
in 12 soils that ranged in organic carbon content from 0.081% to 21.7%.
K values for triclopyr ranged from 12 to 78. Assuming a Massa-
chusetts soil with 2% organic matter, this would give a K, range of 0.24
(high mobility) to 1.56 (low mobility). As part of the same study, the
mobility of the degradate trichloropyridinol was studied on three un-
specified soils. The K 's ranged from 114 to 156, which in a soil with
2% organic matter would give K,'s of 2.28 (low mobility) to 3.12 (nearly
immobile ) .
Norris et al. (1976) studied the losses due to runoff. Triclopyr was
applied as the TEA salt at the rate of 3 lb /acre to an area where 150
cm of rain fell in 9 months. Residues of 6 ppb and 1 ppb in runoff
11-179
water were measured 5 months and 9 months, respectively, after
application .
TRW (1981) states that triclopyr "is not considered a persistent
compound in soils." However, the available information suggests that
triclopyr can be viewed as somewhat persistent. MuUison (1979) states
that triclopyr has an average half-life of 46 days in soil, depending on
soil type and climatic conditions (no additional data provided) .
Degradation to trichloropyridinol has a half-life of between 79 and 156
days at 15°C and "less than 50 days" at 25°-35°C (EPA, no publication
date provided [e] ; Regoli and Laskowski, 1974; Laskowski et al. ,
1975). Degradation appears to be 5 to 8 times slower than this under
anaerobic conditions (Bidlack et al. , 1976). After application of 3.36
kg/ha of tricolpyr, Norris et al. (1977) found residues of 350, 172, and
65 ppb afer 6, 9, and 12 months. Degradation of trichloropyridinol to
secondary degradation products was shown to have a half-life of 8 to
279 days in a study using 15 soils from ten major agricultural areas
(MuUison, 1979).
In the review of registration material, EPA (no publication date
provided [e]) states that degradation of triclopyr is primarily by
microbial action. As in most situations of microbial degradation, dry
soils and saturated soils decrease the decomposition rate, while moist
soils increase it (Dow Chemical U.S.A.., 1981).
Persistence in Water
Limited data is available on the fate of triclopyr in water. Triclopyr
does not readily combine with sediments or other organic materials and
will remain in solution once it has entered a body of water (TRW,
1981). Volatilization is insignificant (Dow Chemical U.S.A., 1981).
Hamaker (no date) studied the hydrolysis of triclopyr in a buffered
aqueous solution at pH levels of 5, 7, and 8, at temperatures of 15*^,
25°, and 35°C. He found triclopyr to be stable to hydrolysis for
periods of up to 9 months.
11-180
This same study found only minor amounts of photodegradation
products. This contrasts with two other studies cited by TRW (1981)
which state that photodegradation is rapid and complete, with a half-life
of 10 hours in water at 25°C (Mullison, 1979;). TRW (1981) states that
"photodegradation is a major pathway for the dissipation of triclopyr in
aquatic environments."
Indicators of Potential Ground Water Contamination
Table 11-50 provides information on parameters associated with the
mobility of triclopyr. These parameters, and their associated
thresholds, have been suggested by EPA for use in assessing the
potential for pesticide contamination of ground water. A discussion of
these parameters and thresholds, and the methods for arriving at
designated values for individual herbicides, is presented in the main
body of the report as part of the discussion of the fate of herbicides in
the environment.
TABLE 11-50
INDICATORS OF POTENTIAL GROUND WATER CONTAMINATION:
TRICLOPYR
Indicator
Solubility
K
oc
Speciation at pH 5
Hydrolysis half-life
Photolysis half-life
Vapor pressure
Value for Triclopyr
Threshold
Garlon 3 A : very high;
Garlon 4 : emulsifies
(Dow Chemical U.S.A.)
>30 ppm
105.7
<300-500
Anionic
Anionic
(negatively charged)
Stable (acid)
>6 months
10 hours
1.26 X 10~ mm
>3 days
-2
<10 mm Hg
Hg at 25° C (acid)
* ND = no data.
11-181
4. TOXICITY TO NON-TARGET ORGANISMS
Birds
Dow Chemical U.S.A. (1979, 1981) and MuUison (1979) indicate that
triclopyr and its formulations are of low toxicity to mallard ducks and
®
Japanese and bobwhite quail (LCr^ values for triclopyr, Garlon 3 A and
Garlon 4 ranged from 3278 to 11,622 ppm) . An 8-day LC^q value for
the technical triclopyr was reported by Haagsma (1975) to be greater
than 5000 ppm for mallard ducklings and 3278 ppm for Japanese quail.
Fish
Triclopyr appears to be non-toxic to fish. Dow Chemical U.S.A. (1979)
and Mullison (1979) report 96-hr LC^^ values for bluegill and rainbow
(§)
trout exposed to triclopyr and Garlon 3A ranging from 117 to 891 ppm.
®
Both species were less sensitive to Garlon 3A than to the active
ingredient. A study by Haagsma (1975) cited the 96-hour LC-_ value
for DOWCO 233 to be 148 ppm for bluegill and 117 ppm for rainbow
trout. This study also calculated 96-hr LC-_ values for M-3724 (a
water-soluble formulation of DOWCO 233) to be 471 ppm for bluegill and
240 ppm for rainbow trout.
Lower Aquatic Organisms
In studies reported by Dow Chemical U.S.A. (1979) and by Mullison
®
(1979), Garlon 3A appears to be non-toxic to oysters, with LC-,^
values ranging from 56 to 87 ppm. Garlon 3 A was also non-toxic to
shrimp and crabs, with LCj-^ values of 895 ppm and >1000 ppm,
respectively .
Soil Microorganisms
A study by Griffith (1976) showed triclopyr to be non-toxic to six soil
microorganisms: Aerobacter aerogenes. Salmonella typhosa, Staphyloccus
aureus, Pseudomonas aeruginosa, Aspergillus terreus, and Pullularia
pullulams . After 72 hours of incubation with 500 ppm, no apparent
effect was observed when compared to a control. A field study by
Hallborn and Bergman (1979) showed that the rate of nitrogen fixation
11-182
of the lichen Peltigera praetextata and its free-living phycobiant algae
®
Nostoc sp. was not significantly affected by treatment with Garlon 3 A
at rates typically used in forestry applications.
Potential for Bioaccumulation
Triclopyr and its degradates trichloropyridinol and trichloromethoxy-
pyridine did not accumulate in edible portions of catfish or in fish
heads, viscera, or skins in a study by Hedelund (1972). This study
also showed that mosqmto fish did not accumulate significant concen-
trations of the residue trichloropyridinol.
Toxicity Data Evaluation
More publicly available information is needed on the carcinogenic,
mutagenic, and teratogenic effects of triclopyr before conclusions can
be drawn. EPA is currently reviewing its data base on triclopyr and
will be identifying data gaps to be filled.
One chronic oral study on triclopyr was done by IBT . EPA considered
portions of this study to be valid and decided that the study could be
used for supplemental information. Dow Chemical U.S.A. has since
replaced the study.
11-183
BIBLIOGRAPHY
B-1
B-2
Adams, J.B. 1960. Effects of spraying 2,4-D amine on coccinellid
larvae. Can. J. Zool. 38: 285. As cited by USDA (1973).
Adler, I. D. 1980. A review of the coordinated research effort on the
comparison of test systems for the detection of mutagenic effects,
sponsored by E.E.C. Mutation Research 74:77-93.
Affiliated Medical Research, Incorporated, 1974a. Acute Oral Toxicity
in Rats of CGA-24705-6E: Contract No. 121-2255-34. CDL:
112840-B. Unpublished study prepared for Ciba-Geigy Corp.,
Greensboro, N.C. As cited by EPA (1980).
Affiliated Medical Research, Incorporated, 1974b. Acute Dermal LDcn o^
CGA-24705-Technical in Rabbits: Contract No. 120-2255-34. CDL:
112840-E. Unpublished study prepared for Ciba-Geigy Corp,
Greensboro, N.C. As cited by EPA (1980).
Affiliated Medical Research, Incorporated, 1974c. Primary Dermal
Irritation of CGA-24705-6E in Albino Rabbits. Contract No.
121-2255-34. CDL: 112840-J. Unpublished study prepared for
Ciba-Geigy Corp., Greensboro, N.C. As cited by EPA (1980).
Affiliated Medical Research, Incorporated, 1974d. Emetic Dose^r, in
bl)
Beagle Dogs with CGA-24705-6E: Contract No. 121-2255-34. CDL:
112840-D. Unpublished study prepared for Ciba-Geigy Corp.,
Greensboro, N.C. As cited by EPA (1980).
Ahmed, F.E., N.J. Lewis and R.W. Hart, 1977. Pesticide induced
ouabain resistant mutants in Chinese hamster V79 cells. Chem.
Biol. Interactions. 19: 369-74.
Alabaster, J.S. 1969. Survival of fish in 164 herbicides, insecticides,
fungicides, wetting agents and miscellaneous substances.
International Pest Control 11:29-35.
B-3
Aldrich, R.J. and C.J. Willard, 1952. Factors affecting the
pre-emergent use of 2,4-D in corn. Weeds. 1: 338-45. As cited
by NRCC (1978).
Allen, T.J., and C.J. Scifres, 1971. Dicamba Residues in Water:
Dissipation and Influence on Growth of Crop Seedlings. Annual
Report to Velsicol Chemical Corp., May 1, 1971: 1-42. As cited
by Velsicol Chemical Corp. (1981).
Altom, J.D. and J.F. Stritzke, J.F., 1973 Degradation of dicamba,
picloram, and four phenoxy herbicides in soils. Weed Sci. 21:
556-60. As cited by NRCC (1978).
Aly, O.M. and S.D. Faust, 1964. Studies on the fate of 2,4-D and
ester derivatives in natural surface waters. J. Agric. Food
Chem. 12(6): 541-6. As cited by TRW (1981).
Ambrose, A.M. 1943. Studies on the physiological effects of sulfamic
acid and ammonium sulfamate. Jour. Indus. Hyg. and Toxicol.
25(l):26-8.
American National Standards Institute, 1976. Common name for the pest
control chemical
2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-l-methylethyl)
acetamide "metolachlor" . In: ANSI, American National Standard:
ANSI, K62, 198-1976, New York, New York. As cited by EPA
(1980).
Anderson, K.J., E.G. Leighty, and M.T. Takahashi. 1972. Evaluation
of herbicides for possible mutagenic properties. J. Agr. Food
Chem. 20(3):649-56.
Andus, L.J., 1964. The Physiology and Biochemistry of Herbicides.
Academic Press, pp. 104-206. As cited by USDA (1973).
B-4
Aner, D.H., L.E. Cliburn, D.R. Thomas, and J.D. Manner. 1976. The
use of fire, fertilizer, and seed for right-of-way maintenance in
the southeastern United States. In Tillman, R. , ed., Proc. First
National Symposium on Environmental Concerns in Rights-of-Way
Management. Mississippi State University, pp. 155-66.
Archipor, G.N. and I.N. Kozlova 1974. Study of the carcinogenic
properties of the herbicide amine salt of 2,4-D. Voprosy Pitaniya
5:83-4.
Armed Forces Pest Management Board, 1980. Pesticide Spill Prevention
and Management. Technical Information Memorandum No. 15. Ad
Hoc Committee on Pesticide Spill Prevention.
Armstrong, D.E., G. Chesters, and R.F. Harris, 1967. Soil Sci. Soc.
Amer. Proc. 31: 61. As cited by TRW (1981).
Ami, P. and D. Miller, 1976. Salmonella/ Mammalian-Microsome
Mutagenicity Test with CGA 24705 (Test for Mutagenic Properties
in Bacteria): PH 2.632. CDL: 95768-B. UnpubHshed study
received Jan. 19, 1977 under 7F1913; prepared by Ciba-Geigy,
LTD., Basle, Switzerland. As cited by EPA (1980).
Arnold, W.R., P.W. Santelmann, and J.Q. Lynd, 1966. Picloram and
2,4-D effects with Aspergillus niger proliferation. Weeds 14:
89-90. And as cited by TRW (1981).
Arthur D. Little, Inc. 1979. Environmental Construction and
Maintenance Study of High-Voltage Transmission Facility Corridors.
Report to Commonwealth of Massachusetts Energy Facilities Siting
Council, Cambridge, MA.
Ashton, F.M., 1961. Movement of herbicides in soil with simulated
furrow irrigation. Weeds 9: 612-9. As cited by Majka (1976).
B-5
Atkins, E.L. Jr., E. Greywood and R. MacDonald. 1975. Toxicity of
Pesticides and other Agricultural Chemicals to Honey Bees
Laboratory Studies. Leaflet 2287 University of California, Division
of Agricultural Studies, Riverside, California.
Atkins, E.L. Jr., L.D. Anderson, D. Kellura and K.W. Neuman. 1976.
Protecting Honey Bees from Pesticides. University of California,
Division of Agricultural Sciences Leaflet 2883., Riverside.
Audus, L.J., 1951. The biological detoxification of hormone herbicides
in soil, vol. 3, p. 170-92. As cited by USDA (1973), (No journal
title was provided) .
Audus, L.J. 1976. Herbicides Physiology, Biochemistry, Ecology. Vol.
2. , 2nd edition. Academic Press, New York, NY.
Aulicino, F. , M. Bignami, A. Carere, G. Contin, G. Morpurgo and A.
Velcich, 1976. Mutational studies with some pesticides in
Aspergillus nidulans. Mutat. Res. 38(2): 138.
Auyama, M. 1975. Effect of anti-flame treating agents on the skin.
Nagoya Med. J. 20(1): 11-19.
Axelson, D., C. Edling, H. Kling, E. Anderson, C. Hogstedt and L.
Sundell. 1979. Updating of the mortality among pesticide-exposed
railroad workers. Lakartidningen 76:3505-6.
Aziz, S.A., 1974. Photolysis of CGA-24705 on soil slides under
National and Artificial Sunlight Conditions: GAAC-74102. CDL:
94385- J. Unpublished study prepared by Ciba-Geigy Corp.,
Greensboro, N.C. As cited by EPA (1980).
Aziz, S.A., and R.A. Kahrs, 1975. Photolysis of CGA-24705 in
Aqueous Solution - Additional Information: GAAC-75021. CDL:
94385-M. Unpublished study prepared by Ciba-Geigy, Corp.,
Greensboro, N.C. As cited by EPA (1980).
B-6
Bakshi, K.S., D.J. Brusick and D.D. Sumner. 1981. Mutagenic
activity of corn plants grown in untreated and atrazine. Aatrex
treated soil. Abstract no. P4. Environ. Mutagenesis. 3:302-3.
Balasubramanian, A., and G. Rangaswami. 1973. Influence of foliar
application of chemicals on the root exudations and rhizosphere
microflora of Sarum Vulgare and Crotolaria juncea. Folia
Microbiol., 18: 492-8.
Baldwin, B.C., and M.F. Bray, and M.J. Geochegan, 1966. The
microbial decomposition of paraquat. Biochem. J. 101: 15P. As
cited by Simsiman, et al. (1976).
Ballantine, L.G., 1975. CGA-24705. Environmental Impact Statement:
GAAC-75011-CDL: 94385-A, 94376. Unpublished study received
Mar. 26, 1975 under 5F1606; prepared by Ciba-Geigy Corp.,
Greensboro, N.C. As cited by EPA (1980).
Bamford, D., M. Sorsa, U. Gripenberg, I. Laamanen and T. Meretoja
1976. Mutagenicity and toxicity of Amitrole III. Microbial tests.
Mutation Research 40:197-202.
Barnett, A. P., E.W. Hauser, A.W. White, and J.H. HoUaday. 1967.
Loss of 2,4-D in washoff from cultivated fallow land. Weeds 15:
133-7. As cited by NRCC (1978).
Barrows, M.E., 1974. Exposure of fish to 14C-CGA-24705.
Accumulation, Distribution, and Elimination of 14C Residues.
Report No.: 73019-3. Received March 27, 1975 under SF1606.
CDL: 94376-E. Unpublished study prepared by EG&G Bionomics
Environmental Consultants for Ciba-Geigy Corp., Greensboro,
N.C. As cited by EPA (1980).
Barthel, E. 1981. Increased risk of long cancer in pesticide-exposed
male agricultural workers. Journal of Toxicology and Environmental
Health. 8:1027-40.
B-7
Basrur, S.V., R.N. Fletcher and P.K. Basrur. 1976. In vitro effects
of 2,4-dichlorophenoxy acetic acid (2,4-D) on bovine cells. Can J.
Comp. Med. 40(4) :408-15.
Bathe, R., 1973. Acute Oral LD^^ of Technical CGA-24705 in the Rat:
bu
Project No. Siss 2979. CDL: 112840-A. Unpublished study-
prepared by Ciba-Geigy Corp., LTD., Basle, Switzerland. As
cited by EPA (1980).
Bauer, K. 1961. Studren uber Nebenwirkungen von Pflanzen-
schutzmitteln auf Fische und Fischnahrtiere Mitt. biol. Bunde-
sanstalt Land u Forstwirtsch, Berlin-Dahlem 105, 5. As cited by
USDA (1973).
Baur, J.R., 1978. Movement in Soil of Tebuthiuron from Sprays and
Granules. Texas Ag . Exp. Sta. Pub. PR-3524, 14pp. As cited
by Reed (1982).
Baur, J.R., R.W. Bovey , and M.G. Merkle, 1972. Concentration of
picloram in runoff water. Weed Science 20: 309-13. As cited by
TRW (1981); NRCC (1974).
Beasley, P.G. 1966. Dipyridylium Residues in an Aquatic Environment.
Ph.D. Thesis. Auburn University, Auburn, AL
Bednarz, T. , and J. Zarnouski, 1980. Abstract from Proc. Int. Conf,
Bioindic. Deter. Reg. 39-41. As cited by MACC (1982).
Behrens, P., and W.E. Lueschen, 1979. Dicamba volatility. Weed Sci.
27(5): 486-93. As cited by TRW (1981).
Bell, G.R., 1957. Some morphological and biochemical characteristics of
a soil bacterium which decomposes 2 , 4-dichlorophenoxy acetic acid.
Canadian Journal of Microbiology 3: 821-40. As cited by USDA
(1973).
B-8
Bell, G.R., 1960. Studies on a soil Achromobacter which degrades
2 , 4-dichlorophenoxy acetic acid. Canadian Journal of Microbiology
6: 325-37. As cited by USDA (1973).
Benigni, R. , M. Bignami, A. Carere, P. Comba, G. Conti, L. Conti,
R. Crebelli, E. Dogliotti, G. Gualandi, A. Novelletto, and V.A.
Ortali. 1979. Mutagenicity studies in Salmonella , Streptomyces,
Aspergillus and unscheduled DNA synthesis in EUE cells of
paraquat and diquat. Abstract no. 42. Mutation Research 64:127-8.
Best, J.A. , J.B. Weber, and T.J. Monaco, 1975. Influence of soil pH
on s-triazine availability to plants. Weed Science 26: 378-82. As
cited by TRW (1981).
Bidlack, H.D., et al. , 1976. Comparison of the Degradation Rates and
Decomposition Products of 14p triclopyr in Aerobic and Waterlogged
Soil. Report No. GM-C-919. June 22. As cited by TRW (1981).
Biggar, J.W., and M.W. Cheung, 1973. Adsorption of picloram
(4-amino-3,5,6-trichloropicolinic acid) on Panoche, Ephrata and
Palouse soils: A thermodynamic approach to the adsorption
mechanism. Soil Sci. Soc. Amer. Proc. 37: 863-8. As cited by
TRW (1981).
Bignami, M.F. Aulicino, A. Velcich, A. Carere, and G. Morpurgo.
1977. Mutagenic and recombinogenic action of pesticides in
Aspergillus nidulans. Mutation Research 46:395-402.
Birk, L.A., and F.E.B. Road-House, 1962. Penetration of and
persistence in soil of the herbicide atrazine. Canadian Journal of
Plant Science 44: 21-7. As cited by TRW (1981).
Bjerke, E.L., J.L. Herman, P.W. Miller, and J.H. Wetters. 1972.
Residue study of phenoxy herbicides in milk and cream. J. Agric.
Food Chem. 20: 963-7.
B-9
Bjorklund, N.-E., and K. Erne. 1966. Toxicological studies of phen-
oxyacetic herbicides in animals. Acta. Vet. Suand. 7: 364-90.
Bjorn, M.K., and H.T. Northen, 1948. Effects of 2 ,4-dichlorophen-
oxy acetic acid on chicks. Science 108: 479-80. As cited by NRCC
(1978).
Black, W.J.M., A. Calderbank, G. Douglas, and R.H. McKenna. 1966.
Residues in herbage and silage and feeding experiments following
the use of diquat as desiccant. J. Sci. Food Agr. 17: 506. As
cited by Simsiman, et al. (1976).
Blackborn, R.D., and L.W. Weldon, 1963. Results of 3 years of
testing diquat as an aquatic herbicide in Florida. Proc. S. Weed
Control Conf. 16: 365. As cited by Simsiman, et al (1976).
Bohmont, B.L., 1967. Toxicity of herbicides to livestock, honey bees,
and wildlife. Proc. W. Weed Control. Conf. 21: 25. As cited by
Simsiman, et al. (1976).
Bond, C.E., R.H. Lewis, and J.L. Fryer, 1959. Toxicity of various
herbicidal materials to fishes. In: Biological Problems in Water
Pollution. Trans. 1959 Sem. U.S.H.E.W., pp. 96-101. As cited
by USDA (1973).
Bond, C.E., R.H. Lewis, and J.L. Fryer, 1960. Toxicity of various
herbicidal materials to fishes. Trans. 1959 Seminar: Biological
problems in water pollution, pp. 96-101. The Robert A. Taft
Engineering Center, Tech. Rept. W60-3. Public Health Service,
U.S. Department of Health Education and Welfare, Cincinnatic,
Ohio. As cited by Simisiman, et al. (1976).
Bontoyan, W.R., M.W. Law, and D.P. Wright, Jr. 1979. Nitrosamines
in agricultural and home-use pesticides. J. Agric. Food Chem.
27(3):631-5.
B-10
Boutwell, R.K., and D.K. Bosch. 1959. The tumor-promoting action of
phenol and related compounds for mouse skin. Cancer Research
19:413-24.
Bovey, R.W., and C.J. Scifres, 1971. Residual Characteristics of
Picloram in Grassland Ecosystems. Texas Agricultural Experiment
Station, B-1111, 24 pp. As cited by TRW (1981).
Bovey, R.W., F.S. Davis, and M.G. Merkle. 1967. Distribution of
picloram in Huisache after foliar and soil applications. Weeds 15:
245-9. As cited by TRW (1981).
Bovey, R.W., E. Burnett, R.E. Meyer, C. Richardson, and A. Loh,
1978. Persistence of tebuthiuron in surface runoff water, soil,
and vegetation in the Texas Blackland Prairie. J. Environ. Qual.
7(2): 233-6. As cited by Reed (1982).
Bovey, R.W., et al, 1978. Loss of spray and pelleted picloram in
surface runoff water. Journal of Environmental Quality 7(2):
1978-80. As cited by TRW (1981).
Bowes, G.G., 1972. Personal communication to Dr. R. Grover. As
cited by NRCC (1974).
Brady, N.C., 1974. The Nature and Properties of Soils; 8th Edition.
MacMillan Publishing Co., New York, New York.
Bramble, W.C., and W.R. Byrnes. 1972. A Long-Term Ecological Study
of Game Food and Cover on a Sprayed Utility Right-of-Way .
Purdue University Agric. Exp. Stn. Res. Bull. no. 885. 20 pp.
Bramble, W.C., and W.R. Byrnes. 1976. Development of a stable, low
plant cover on a utility right-of-way. In: Tillman, R. , ed. Proc.
First National Symposium on Environmental Concerns in
Rights-of-Way Management. Mississippi State University. pp.
167-76.
B-11
Bramble, W.C., and W.R. Byrnes. 1982. Development of Wildlife Food
and Cover on and Electric Transmission Right-of-Way Maintained
by Herbicides: A 30-Year Report. Dept. Forestry and Natural
Resources, Agric. Exp. Stn,, Purdue University, West Lafayette,
Indiana.
Braun, R. , J. Schoneich, and D. Ziebarth. 1977. In vivo formation of
N-nitroso compounds and detection of TA1950 mutagenic activity in
the host-mediated assay. Cancer Research 37:4572-9.
Brians, R.D. 1964. The classification of herbicides and type of
toxicity. In: Audus, L.J., ed. , The Physiology and Biochemistry
of Herbicides, Academic Press, New York, New York.
Brightwed, B.B., and J.M. Malik (no date provided). Data provided
by Monsanto Company, Monsanto Agricultural Research Department,
St. Louis, Missouri. In: Environmental Fate File, Glyphosate,
U.S. EPA, Washington, D.C. As cited by TRW (1981).
Bromley, S.W. 1935. The original forest types of southern New
England. Ecol. Monogr. 5:63-89.
Brown, E. , and Y.A. Nishioka, 1967. Pesticides in selected western
streams — A contribution to the national program. Pesticides
Monitoring J. 1(2): 38-46. As cited by USDA (1973).
Buccafusco, R. J. , 1978a. Acute Toxicity Test Results of CGA-24705 to
Bluegill Sunfish (Lepomis macrochirus) . Report #BW-78-181.
Received July 13, 1978 under 100.597. CDL: 234396. Unpublished
study prepared by EG&G, Bionomics; submitted by Ciba-Geigy
Corp., Greensboro, N.C. As cited by EPA (1980).
Buccafusco, R.J., 1978b. Acute Toxicity Test Results of CGA-24705 to
Rainbow Trout (Salmo gairdneri) . Report #BW-78-6-186. Received
July 13, 1978. Under 100-597. CDL: 234396. Unpublished study
B-12
prepared by EG&G, Bionomics, submitted by Ciba-Geigy Corp.,
Greensboro, N.C. As cited by EPA (1980).
Buchanon, G.A., and H.E. Hiltbold, 1973. Performance and
persistence of atrazine. Weed Science 21: 412-6. As cited by
TRW (1981).
Buck, W.B., W. Binns, L. James, and M.C. Williams. 1961. Results of
feeding of herbicide-treated plants to calves and sheep. J. Amer.
Vet. Med. Assoc. 138: 320. As cited by USDA (1973).
Buffington, J.D. 1974. Assessment of the Ecological Consequences of
Herbicide Use along Transmission Line Rights-of-Way and
Recommendation for such use. Argonne National Laboratory,
Publication No. ANL/ES-34. Argonne, XL.
Burcar, P.J., R.L. Wershaw, M.C. Goldberg, and L. Khan. 1966.
Gas chromatographic study of the behavior of the iso-octyl ester of
2,4-D under field conditions in North Park, Colorado. Anal.
Instrum. 4: 215-24. As cited by NRCC (1978).
Burger, K., I.C. MacRae, and M. Alexander. 1962. Decomposition of
phenoxyalkyl carboxylic acids. Proc. Soil Sci. Soc. Am. 26:
243-6. As cited by NRCC (1978).
Burkhard, N., 1974. CGA-24705: Hydrolysis of CGA under Laboratory
Conditions: AC 2.5.53; SPR 2/74 CDL: 94222-H. Unpublished
study prepared by Ciba-Geigy Ltd., Basle, Switzerland. As cited
by EPA (1980).
Burnett, E. , and C.W. Richardson, 1980. Herbicide residues in runoff
water, soils and vegetation. USDA Grassland Soil and Water
Research Laboratory, Temple, Texas. In: Toxicology Research
Projects Directory Research Abstract, vol. 5, issue no. 9. As
cited by TRW (1981).
B-13
Burnside, O.C., and T.L. Lavy , 1966. Dissipation of dicamba. Weeds
14: 211-14. As cited by EPA (1975).
Burnside, O.C., G.A. Wicks, and C.R. Fenster, 1971. Dissipation of
dicamba, piclorara, and 2,3,6-TBA across Nebraska. Weed Science
19: 323-5. As cited by NRCC (1974).
Burschel, P. and V.M. Freed, (no publication date provided). The
decomposition of herbicides in soils. Weeds 7: 157-61. As cited
by TRW (1981). reference no. 30.
Butler, P. A., 1965. Effects of herbicides on estuarine fauna.
Presented at 13th Annual meeting of Southern Weed Conference,
January 19-21, Dallas, Texas. As cited by TRW (1981).
Butler, P. A., 1965a. Effects of herbicides on estuarine fauna. Proc.
Southern. Weed Conference 18: 576-80. As cited by TRW (1981).
Cain, D.S., 1966. An investigation of the Herbicidal Activity of
2-Methoxy-3, 6-Dichlorobenzoic Acid. Ph.D Thesis, University of
Illinois, Urbana, Illinois. As cited by USDA (1973).
Calderbank, A., 1968. The bipyridylium herbicides. Adv. Pest
Control Res. 8: 127. As cited by Simsiman, et al. (1976).
Call, D.J., Rikent, and L.T. Brooke. 1979. Estimates of "No Effect"
Concentrations of Selected Pesticides in Freshwater Organisms.
Third Quarterly Progress Report to EPA, January 1-March 31.
Cameron, J.J., and J.W. Anderson, 1977. Results of the Stream
Monitoring Program Conducted During FY 1977 Herbicide Spray
Project - Coos Bay District USDI/BLM Report, Coos Bay, OR. As
cited by TRW (1981).
B-14
Carer e, A., V.A. Ortali, G. Cardamone, A.M. Torracca, and R.
Raschetti. 1978. Microbiological mutagenicity studies of pesticides
in vitro. Mutation Research 57:277-86.
Carmelli, D., L. HofLerr, J. Tomsic, and R. Morgan. 1981. A
Case-Control Study of the Relationship between Exposure to 2,4-D
and Spontaneous Abortions in Humans. SRI International, Palo
Alto, CA.
Caro, J.H., H.P. Freeman, and B.C. Turner, 1974. Persistence in soil
and losses in runoff of soil-incorporated carbaryl in a small
watershed. J. Agric. Food. Chem. 22(5): 860-3. As cited by TRW
(1981).
Carter, M.C., 1969. Amitrole. In: Kearney, P.C., ed. , Degradation
of Herbicides, pp. 187-206.
Carter, M.S., 1975. Amitrole. In: Kearney, P.C., and D.D.
Kaufman, eds.. Herbicides: Chemistry, Degradation and Mode of
Action, 2nd ed. , Marcel Dekker, Inc., New York, New York, pp.
377-98. As cited by TRW (1981).
Carvell, K.L. 1973. Environmental Effects of Herbicides Phase 1 Report
of Edison Electric Institute. EEI Publication No. 72-963, New York,
New York.
Chandra, P. 1964. Herbicidal effects on certain soil microbial activities
in some brown soils of Saskatchewan. Weed Research 5: 54-63.
Chandra, T., W.R. Furtick, and W.B. Bollen, 1960. The effect of four
herbicides on microorganisms in nine Oregon soils. Weeds 8: 589.
As cited by Gangstad (1982).
Chang, S.S., and J.F. Stritzke, 1977. Sorption, movement, and
dissipation of tebuthiuron in soils. Weed Sci. 25: 184-7. As cited
by Reed (1982).
B-15
Chevron Chemical Company. 1982. Material Information Bulletin for
ORTHO Diquat 2 Spray. Richmond, California.
Chirchirillo, M.T., 1966. Photochemical conversion of Banvel D to 5-OH
Banvel. Internal corespondence to D.L. Watson, September 21.
As cited by Velsicol Chemical Corp. (1981).
Choi, K.L., S.S. Que Hee, and R.G. Sutherland, 1976. 2,4-D levels
in the South Saskatchewan River in 1973 as determined by a GLC
method. J. Environ. Sci. Health Bll: 179-83. As cited by NRCC
(1978).
Chollet, M.C., N. Degraeve, J. Gilot-Delhalle, A. Colizzi, J.
Moutschen, and M. Moutschen-Dahmen. 1982. Mutagenic efficiency
of atrazine with and without metabolic activation. Abstract no. 2.
Mutation Research 97:237-8.
Christensen, CD., M.L. Jones, and G.J. Shoop, 1974. Tebuthiuron
for total vegetation control on rights-of-way and industrial sites.
Proc. N.E. Weed Sci. Soc. 28: 341-6. As cited by Reed (1982).
Christensen, H.E., T.T. Luginbyhl, and B.S. Carroll (eds.), 1974.
Toxic Substances List. National Institute for Occupational Safety
and Health. HEW Publication No. (NIOSH) 74-134. Govt. Printing
Office, Washington, D.C. As cited by Arthur D. Little, Inc.
(1979).
Chrzanowski, R.L. 1983. Metabolism of [14C] fosamine ammonium brush
and turf. J. Agric. Food Chem. 31(2):223-7.
Chrzanowski, R.L., J.C-Y. Han, and C.L. Mcintosh. 1979. Metabolism
of [14C] fosamine ammonium in the rat. J. Agric. Food Chem.
27(3):550-4.
B-16
Ciba-Geigy, 1971. Aatrex Herbicide Technical Bulletin. GAC700-564.
Geigy Agricultural Chemicals. Greensboro, N.C. As cited by
TRW (1981).
Ciba-Geigy Limited, 1976. Dominant Lethal Study on CGA 24705
Technical: Mouse (Test for Cyto-Germinal Cells) PH 2.632. CDL:
96717-C; 96717-D. Unpublished study including Addendum;
received January 18, 1978 under 7F1913. As cited by EPA (1980).
Clark, D.E., J.E. Young, R.L. Younger, L.M. Hunt, and J.K.
McLaran, 1964. The fate of 2,4-dichlorophenoxyacetic acid in
sheep. J. Agric. Food Chem. 12: 43-5.
Clemens, H.P., and K.E. Sneed. 1959. Lethal Doses of Several
Commercial Chemicals for Fingerling Channel Catfish. U.S. Fish
and Wildlife Service. Special Scientific Report. Fisheries no. 316. 10
pp.
Coakley, J., J. Campbell, and E. McFarren. 1964. Determination of
butoxyethanol ester of 2,4-D in shellfish and fish. J. Agr. Fd.
Chm. , 12: 262-5.
Coats, G.E. and H.H. Funderburk, Jr., J.M. Lawrence, and D.E.
Davis, 1964. Persistence of diquat and paraquat in pools and
ponds. Proc. S. Weed Control Conf. 17: 304. As cited by
Simsiman, et al. (1976).
Coats, G.E., H.H. Funderbank, Jr., J.M. Lawrence, and D.E. Davis,
1966. Factors affecting persistence and inactivation of diquat and
paraquat. Weed Research 6: 58. As cited by Simsiman, et al.
(1976).
Coddington, J., and K.S. Field, 1978. Rare and Endangered Vascular
Plant Species in Massachusetts. New England Botanical Club in
cooperation with U.S. Fish and Wildlife Service, Newton Corner,
MA.
B-17
Cody, J.B. 1975. Vegetation Management on Power Line Rights-of-Way.
A State of the Knowledge Report. Research Report No. 28.
Applied Forestry Research Institute. Syracuse, New York.
Cody, W.J., I.V. Hall, and C.W. Crompton, 1977. The biology of
Canadian weeds. 26. Dennstaedtia Punctilobula (Michx.) Moore.
Can. J. PI. Sci. 57:1159-68.
Coffey, D.L., and G.F. Warren, 1969. Inactivation of herbicides by
activated carbon and other adsorbants. Weed Sci. 17: 16-9. As
cited by NRCC (1978).
Cohen, A.J., and P.O. Grasso. 1981. Review of the hepatic response
to hypolipidgenic drugs in rodents and assessment of its
toxicological significance to man. J. Cosmet. Toxicol. 19:585-605.
Collins, T.F.X., and C.H. Williams, 1971. Teratogenic studies with
2,4,5-T and 2,4-D in the hamster. Bull. Environm. Contam.
Toxicol. 6: 559-67.
Cooke, A.S., 1972. The effects of DDT, dieldrin and 2,4-D on
amphibian spawn and tadpoles. Environ. Pollut. 3: 51-68. As
cited by NRCC (1978).
Cope, O.B., 1965. Some response of fresh-water fish to herbicides.
Proc. 18th S. Weed Control Conf . , p. 439. As cited by USDA
(1973).
Cope, O.B., 1966. Contamination of the freshwater ecosystem by
pesticides. J. Applied. Ecol. 3: 33. As cited by Simsiman, et al.
(1976).
Corbin, F.T., and R.P. Upchurch, 1967. Influence of pH on
detoxification of herbicides in soil. Weeds 15: 370-7. As cited by
TRW (1981).
B-18
Corbin, F.T., R.P. Upchurch, and G.R. Stephenson, 1971. Jour.
Agric. Food Chem. 19: 1183. As cited by Velsicol Chemical Corp.
(1981).
Council for Agricultural Science and Technology. 1978. Report No. 77.
The Phenoxy Herbicides, 2nd edition, 28 pp.
Courtney, K.D., 1977. Prenatal effects of herbicides: evaluation by
the prenatal development index. Arch. Envir. Contam. Toxicol
6(1): 33-46.
Cowley, G.T. and E.P. Lichtenstein. 1970. Growth inhibition of soil
fungi by insecticides and annulment of inhibition by yeast extract
or nitrogenous nutrients. Journal of General Microbiology 62:27-34.
Crafts, A.S., 1949. Toxicity of 2,4-D in California soils. Hilgardia
19: 141-58. As cited by NRCC (1978).
Crosby, D.G. and R.K. Tucker, 1966. Toxicity of aquatic herbicides
to Daphnia magna. Science 154: 289-91.
Curtis, M.W. and C.H. Ward, 1981. J. of Hydrology 51: 359. As
cited by MACC (1982); no title provided.
Dalton, R.L., A.W. Evans, and R.C. Rhoades. 1966. Disappearance of
diuron from cotton field soils. Weeds 14: (1)31-3.
Damanakis, M. , D.S.H. Drennan, J.D. Fryer, and K. Holly, 1970.
The adsorption and mobility of paraquat on different soils and soil
constituents. Weed Research 10: 264. As cited by Simsiman, et
al. (1976).
Daniel, J.W., and J.C. Gage, 1966. Absorption and excretion of diquat
and paraquat in rats. Brit. J. Ind. Med. 23: 133. As cited by
Simsiman, et al. (1976) and Rose et al. (1980).
B-19
Davidson, J.M., and R.K. Chang, 1979. Transport of picloram in
relation to soil physical conditions and pore-water velocity. In:
Proc. Southern Weed Science Society 32: 182-97. As cited by TRW
(1981).
Davies, P.J.T., 1964. Uptake, movement, and physiological activities
of 1, l'-ethylene-2,2'-dipyridylium dichloride in submerged aquatic
plants. M.S. Thesis, University of California, Davis, CA As
cited by Simsiman, et al. (1976).
Day, B.E., et al. , 1961. The decomposition of amitrole in California
soils. Weeds 9(3): 443-56. As cited by TRW (1981).
De Rose, H.R., 1946. Persistence of some plant-growth-regulators
when applied to the soil in herbicidal treatments. Bot. Gaz. 107:
583-9. As cited by NRCC (1978).
De Rose, H.R., and A.S. Newman, 1948. The comparison of the
persistence of certain plant-growth-regulators when applied to soil.
Proc. Soil Sci. Soc. Am. 12: 222-6. As cited by NRCC (1978).
DeBach, P. 1974. Biological Control by Natural Enemies. Cambridge
University Press, Cambridge, England.
De Bertoldi, M. , M. Griselli, M. Giovannetti, and R. Barale. 1980.
Mutagenicity of pesticides evaluated by means of gene-conversion
in Saccharomyces cerevisiae and in Aspergillus nidulans.
Environmental Mutagenesis 2:359-70.
Department of Navy, 1976. Chemical Control of Disease Vectors and
Economic Pests, Naval Air Station, Jacksonville, FL As cited by
Gangstad (1982).
Desteven, D., 1982. Seed production and seed mortality in a temperate
forest shrub; witch hazel (Hamamelis virginiana) . J. Ecol. 70:
. 437-44.
B-20
DeVaney, T.E., 1968. Chemical vegetation control manual for fish and
wildlife management programs. Bur. Sport Fisheries and Wildlife
Research, Publ. 48, USDI, Washington, D.G. As cited by Carvell
(1973).
DHEW, 1979. Affirmation of GRAS status as an indirect human food
ingredient. Federal Register 44(31), February 13.
Dionne, E. , 1978. Chronic Toxicity of CGA-24705 to the Fathead
Minnow (Pimep hales promelas) . Received 12-13-78 under 100-587.
CDL: 236620, Prepared by EG&G Bionomics for Ciba-Geigy
Corporation, Greensboro, N.C. As cited by EPA (1980).
Dixon, J.B., et al. , 1970. Soil Sci. Soc. Amer. Proc. 34: 805. As
cited by Simsiman, et al. (1976).
•f
Douglass, J.E., D.R. Cochrane, G.W. Bailey, J.I. Teasley , and D.W.
Hill, 1969. Low herbicide concentration found in streamflow after
a grass cover is killed. U.S.D.A. Forest Serv. Res. Note SE-108.
3 pp. As cited by NRCC (1978).
Dow Chemical U.S.A., 1972. Phenoxy Herbicides Reference
Information. Midland, MI As cited by USDOE (1980).
Dow Chemical U.S.A., 1977. Material Safety Data Sheet for 2,4-D.
Midland, Michigan.
Dow Chemical U.S.A., 1979. Technical data sheet for triclopyr, the
active ingredient of garlon herbicides, Midland, MI As cited by
TRW (1981).
Dow Chemical U.S.A., 1980a. Material Safety Data Sheet for Esteron
99. Midland, Michigan.
Dow Chemical U.S.A., 1980b. Material Safety Data Sheet for Formula
40. Midland, Michigan.
B-21
Dow Chemical U.S.A., 1981. (September) .Data supplied to TRW by Dow
Chemical Co., Midland, MI As cited by TRV/ (1981) reference no.
34 on page A-311.
Dow Chemical U.S.A., 1981a. Environmental Considerations for
Triclopyr, Picloram, and 2,4-D. Midland, MI
Drill, V.A., and T. Hiratzka, 1953. Toxicity of 2,4-D and
2,4,5-trichorophenoxy acetic acid. Arch. Ind. Hgy., 7: 61-7.
Dufford, R. , G. Mori De Moro, and A. De Duffard. 1982. Hatching
and lipid composition of chicks brain from eggs treated with
2,4-dichlorophenoxyacetic butyl ester. Toxicology 24:305-11.
Dunachie, J.F., and W.W. Fletcher. 1970. The toxicity of certain
herbicides to hens' eggs assessed by the egg-injection technique.
Ann. Appl. Biol. 66:515-20.
Duncan, W.M. 1935. Root systems of woody plants of old fields of
Indiana. Ecology 16:554-67.
Du Pont, 1967. Technical data sheet for ammonium sulfamate-fish.
Wilmin g ton , D E .
Du Pont. 1972. Technical data sheet for diuron. , Wilmington, DE.
Du Pont. 1972a. Technical data sheet for ammonium sulfamate.,
Wilmington, DE,
Du Pont. 1972b. Material Safety Data Sheet for AMMATE X-Nl Weed
and Brush Killer. Wilmington, DE.
Du Pont, 1975. "Krenite" Brush Control Agent: Technical Information
and Spray Guide. Wilmington, DE. As cited by TRW (1981).
B-22
Du Pont, 1979. Technical data sheet for fosamine ammonium.
Wilmington, DE.
Du Pont, 1979a. Technical data sheet for bromacil. Wilmington, DE.
Du Pont. 1980 (September 5). Information supplied to TRW by Du
Pont, Wilimington, DE. As cited by TRW (1981) reference no. 2
on page A-146.
Du Pont, 1983. Technical data sheet for fosamine ammonium.
Wilmington, DE,
Du Pont, 1983a, Technical data sheet for diuron, Wilmington, DE.
Dupre, G., 1974a. Runoff Characteristics of 14C-CGA-2470 Applied to
Sandy Loam Soil under Greenhouse Conditions: Report no. 73022-1.
CDL: 94222-D. Unpublished study received September 26, 1974
under 561553; prepared by Bio-dynamics Inc. for Ciba-Geigy
Corp., Greensboro, N.C. As cited by EPA (1980).
Dupre, G., 1974b. Abbreviated Anaerobic metabolism of 14C-CGA-24705
in Silt Loam Soil under Greenhouse Conditions: Report No.
73019-3. CDL: 94222-B. Unpublished study received September
26, 1974 under 561553; prepared by Bio/dynamics Inc. for
Ciba-Geigy Corp., Greensboro, N.C. As cited by EPA (1980).
Durham, W.F. and C.H. Williams, 1972. Mutogenic, teratogenic, and
carcinogenic 6022 properties of pesticides. Ann. Rev, Entomol, 17:
123-48.
Edson,, E.F. and D.M. Sanderson, 1965. Toxicity of the herbicides
2-methoxy -3, 6-dichlorobenzoic acid (dicamba) and 2-methoxy -3,
5,6-trichlorobenzoic acid (tricamba) . Fd. Cosmet. Toxicol., 3:
299-304.
B-23
Egler, F.E., 1954a. Vegetation science concepts. I. Initial floristic
composition, a factor in old-field vegetation development. Vegetatio
14:412-17.
Egler, F.E. 1954b. The bald eagle state forest right-of-way,
Pennsylvania: Plants take over future brush control. Proc. Eighth
Annual Meeting Northwest Weed Control. Conf. p. 459-63.
Egler, F.E. and S.R. Foote. 1975. The Plight of the Right-of-Way
Domadn: Victim of Vandalism, 2 volumes. Futura Media Services,
Mt. Kisco, NY.
Ehman, P.J. and J.J. Birdsall, 1963. Fate of cacodylic acid in soils
and plants, contract DA-18-064-CML-2836(A) , Ansul Chemical
Company for U.S. Army Biological Laboratories, Fort Detrick,
Frederick, MD. As cited by Gangstad (1982).
Eisenbeis, S.J., D.L. Lynch, and A.E. Hampel. 1981. The Ames
Mutagen Assay tested against herbicides and herbicide
combinations. Soil Science 131(1): 44-7.
Elanco Products Company, 1980. Product safety data sheet for Spike
5G (tebuthiuron) . , Indianapolis, IN
Elder, J.H., C.A. Lembi and D.J. Morre, 1970. Toxicity of 2,4-D and
Picloram to Fresh Water Algae. NTIS PB-199-114. As cited by
TRW (1981).
EUegehausen, H., 1976a. Project Report 4176: Degradation of CGA
24705 in Aerobic, Anaerobic, and Autoclaved Soil. AC 2.52.
Received February 6, 1978 under 100-583 CDL: 232789-D.
Unpublished study prepared by Ciba-Geigy Ltd., Basle,
Switzerland. As cited by EPA (1980).
Ellegehausen, H., 1976b. Project Report 5/76: Addendum to Project
Report 4/76: Degradation of CGA 24705 in Aerobic, Anaerobic,
B-24
and Autoclaved Soil. AC 2.52. Received February 6, 1978.
Under 100-583. CDL: 232789-E. Unpublished study prepared by
Ciba-Geigy Ltd., Basle, Switzerland. As cited by EPA (1980).
EUegehausen, H. 1977. Project Report 32/77: Uptake Transfer and
Degradation of CGA 24705 (Dual ) by Aquatic Organisms. AC
2.52. Received February 6, 1978 under 100-583. CDL: 232789-C,
Unpublished study by Ciba-Geigy Ltd., Basle, Switzerland. As
cited by EPA (1980).
Ellis, P. A. and N.D. Camper. 1982. Aerobic degradation of diuron by
aquatic microorganisms. J. Environ. Sci. Health. B17(3) :277-89.
Elo, H. and P. Ylitalo. 1977. Substantial increase in the levels of
chorophenosyacetic acids in the CNS of rats as a result of severe
intoxication. Acta. Pharmacol, and Toxicol, 41:280-4.
Embree, J.W., Jr. 1976. Further comments on the assessment of the
mutagenic properties of diquat and paraquat in the murine
dominant lethal test. Mutation Research 31:123-5.
Engelhorn, R. , 1954. Uber den Einflub des Athyl-urethans und des
phenylcarbaminsaure-isopropylesters auf das lungengewebe der
ratte. Arch. Exp. Pathol. Pharmakol, 223: 117. As cited by
Durham and Williams (1972).
EPA, 1975. Initial Scientific and Mini-Economic Review of Dicamba.
Submitted by Arthur D. Little, Inc. Contract No. 68-01-2489,
Office of Pesticide Programs, Washington, D.C.
EPA, 1975a. Production, Distribution, Use and Environmental Impact
Potential of Selected Pesticides. Office of Hazardous Materials,
Washington, D.C. As cited by USDOE (1980).
EPA, 1977. As cited by NRCC (1978); not included in bibliography.
B-25
EPA. 1980. Metolachlor, Pesticide Registration Standard. Office of
Pesticides and Toxic Substances. Washington, DC.
EPA, 1980a. Surveillance Index Document for Bromacil. Prepared April
15 by D.C. Fleming, Food and Drug Administration, Washington,
D.C.
EPA, 1980b (July 30). Surveillance Index Chemistry Data for 2,4-D.
Residue Chemistry Branch, Hazard Evaluation Division,
Washington, D.C. As cited by EPA (1982a).
EPA, 1981. Teratology and Postnatal Studies in Rats of the Propylene
Glycol Butyl Ether and Isooctyl Esters of 2,4-Dichlorophenoxyacetic
Acid. EOPA-600/ 5 1-81-035, Health Effects Research Labatory,
Research Triangle Park, NC.
EPA 1981a. Ammonium sulfamate, pesticide registraion standard. Office
of Pesticides and Toxic Substances, Washington, D.C.
EPA, 1981b. Surveillance Index Support Document: Diuron. , Hazard
Evaluation Division, Washington, D.C. As cited by EPA (1982).
EPA, 1982. Diuron - SI Class III Herbicide (Review of available data).
Prepared by R. Doyle, FDA, Washington, D.C.
EPA, 1982a. 2,4-D: SI Class III Herbicide. Review of available data
prepared November 5 by D. Reed, Food and Drug Administration,
Washington, D.C.
EPA. (no publication date provided [a]) Information based on review of
Ecological Effects Branch registration files. As cited by TRW
(1981) reference no. 14 on page A-40.
EPA. (no publication date provided [b]) Information based on review of
the Registration Files of the Environmental Fate Branch. As cited
by TRW (1981) reference no. 20 on page A-147.
B-26
EPA. (no publication date provided [c]) Information based on a review
of Ecological Effects Branch registration files. As cited by TRW
(1981) reference no. 64 on page A-100.
EPA. (no publication date provided [d]) Information based on a review
of registration files by the Ecological Effects Branch (most
information in this file was originally provided by Monsanto
Company), As cited by TRW (1981) reference no. 16 on page
A-168.
EPA. (no publication date provided [e]) Information based on a review
of registration files of the Ecological Effects Branch. As cited by
TRW (1981) reference no. 9 on page A-309.
EPA. (no publication date provided [f]). Information based on a
review of registration files of the Environmental Fate. As cited by
TRW (1981), reference no. 3 on page A-259.
Epidemiological Studies Laboratory. 1980. 2,4-Dichlorophenoxyacetic
Acid (2,4-D). Evaluation of the Human Health Hazards.
Department of Health Services /Department of Industrial Relations,
State of California.
EPRI. 1978. Environmental Effects of Right-of-Way Management on
Forested Ecosystems. Project 103-3. Palo Alto, CA.
Epstein, S.S, E. Arnold, J. Andrea, W. Basse and Y. Bishop. 1972.
Detection of chemical mutagens by the dominant lethal assay in the
mouse. Toxicology and Applied Pharmocology 23:288-325.
Ercegovich, CD. and D.E.M. Frear, 1965. The fate of
3-amino-l,2,4-triazole in soils. J. Agric. Food Chem. 12(1): 26-9.
As cited by TRW (1981).
Ercegovich, CD., E.R. Bogus, and Buly, R.L. 1978a. The Effects of
5,25, and 125 PPM of metolachlor, [2-Chloro-N-(2-ethyl-6-methylo-
B-27
phenyl) -N-(2-methoxy-l-methylethyl) acetamide] on Actinomycetes,
Bacteria and Fungi in Laboratory Culture Tests. E-2/1-C678.
Received February 6, 1978 under 100-583. CDL: 232789-F, Unpub-
lished report prepared by Pesticide Research Lab . , Pennsylvania
State University for Ciba-Geigy Corp., Greensboro, N.C. As
cited by EPA (1980).
Ercegovich, CD.; R.P. Vallejo, and E.R. Bogus, 1978b. The Effects
of 5,25, and 125 PPM of Metolachlor, [2-Chloro-N-(2-ethyl-6-
methylphenyl)-N-(2-methoxy-l-methylethyl) acetamide], on Soil
Nitrification. E-3/2-CG78. Received February 6, 1978 under
100-583. CDL: 232789-6, Unpublished study prepared by Pesticide
Research Lab, Pennsylvania State University for Ciba-Geigy
Corp., Greensboro, N.C. As cited by EPA (1980).
Erickson, M.D., C.W. Frank, and D.P. Morgan, 1979. J. of Agric.
Food Chem. 27(4): 743-6. As cited by MACC (1982).
Eriksson, M., L. Hardell, N.C. Berg, T. Moller, and O. Axelson.
1981. Soft tissue sarcomas and exposure to chemical substances: a
case-referent study. British Journal of Industrial Medicine
38:27-33.
Erne, K. 1966. Distribution and elimination of chlorinated phen-
oxy acetic acids in animals. Acta Vet. Scand. 7, 240. As cited by
USDA (1973).
Erne, K., 1966a. Determination of phenoxyacetic herbicide in biological
materials. Acta Vet. Scand. 7: 77-96.
Eshel, Y. and G.F. Warren, 1967. A simplified method for determining
phytotoxicity , leaching, and adsorption of herbicides in soils.
Weeds 15: 115-8. As cited by NRCC (1978).
Fahrig, R. , 1974. Comparative mutagenicity studies with pesticides.
lARC Sci. Publ. 10: 161-81
B-28
Fang, S.C., E. Fallin, M.L. Montgomery and V.H. Freed, 1973. The
metabolism and distribution of 2 ,4,5-trichlorophenoxyacetic acid in
female rats. Toxicol. Appl. Pharmacol 24: 555-63.
Farmer, W.J., and Y. Aochi, 1974. Picloram sorption by soils. Soil
Sci. Soc. Amer. Proc. 38: 418-23. As cited by TRW (1981).
Faulkner, J.K., and D. Woodcock, 1964. Metabolism of
2 , 4-dichlorophenoxy acetic acid (2,4-D) by Asperillus niger van
Tiegh. Nature 203: 865. As cited by USDA (1973).
Faulkner, J.K., and D. Woodcock, 1965, Fungal detoxification VII
metabolism of 2,4-dichloro-phenoxy-acetic and 4-chloro-2-methyl-
phenoxy acetic acids by Aspergillus niger. Journal of the Chemical
Society, pp. 1187-91. As cited by USDA (1973).
Fawcett, C.H., J.M.A. Ingram, and R.L. Wain, 1954. The B-oxidation
of w-phenoxyalkylcarboxylic acids in the flax plant in relation to
their plant growth-regulating activity. Proceedings of the Royal
Society of London, 142B: 60-72. As cited by USDA (1973).
Fernald, M.L. , 1950. Gray's Manual of Botany. 8th Edition. D. Van
Nostrand Co. , New York, New York.
Fertig, S.N., 1952. Livestock poisoning from herbicide treated
vegetation. Proc. 6th NE, Weed Control Conf . , p. 13. As cited
by USDA (1973).
Fertig, S.N., 1953. Herbicidal poisoning of livestock. Proc. 7th NE
Weed Control Conf. Suppl. 44. As cited by USDA (1973).
Fink, R., 1974a. Eight-Day Dietary LC-50. Mallard Ducks Technical
CGA-24705. Project No. 108-111. CDL: 112840-0, Unpublished
study prepared by Truslow Farm, Inc. for Ciba-Geigy Corp.,
Greensboro, N.C. As cited by EPA (1980).
B-29
N
Fink, R., 1974b. Eight-Day Dietary LC-50, Bobwhite Quail Technical
CGA-24705. Project No. 108-111. Received September 26, 1974
under 5G1553. CDL: 112840-P, Unpublished study prepared by
Truslow Farm, Inc. for Ciba-Geigy Corp., Greensboro, N.C. As
cited by EPA (1980).
Fink, R., 1978a. One-Generation Study-Bobwhite Quail CGA-24750
Technical Final Report. Received 12-13-78 under 100-587. CDL:
236620, Unpublished report prepared by Wildlife International Ltd.
for Ciba-Geigy Corp., Greensboro, N.C. As cited by EPA (1980).
Fink, R. , 1978b. One-Generation Reproduction Study. Mallard Duck
CGA-24750 Technical Final Report. Received 12-13-78 under
100-587. CDL: 236620, Unpublished report prepared by Wildlife
International Ltd. for Ciba-Geigy Corp., Greensboro, N.C. As
cited by EPA (1980).
Fisher, R.F. 1977. Allelopatic interference among plants. I. Ecological
significance. Proc. Fourth North American Forest Biology
Workshop, State University of New York, College of Environmental
Science and Forestry, Syracuse, New York. pp. 73-92.
Fisher, R.F., R.A. Woods, and M.R. Glavicic. 1978. Allelopatic effects
of goldenrod and aster on young sugar maple. Can. J. For. Res.
8:1-9.
Fitzgerald, C.H., 1966. The degradation of 2 ,4,5-trichlorophenoxy-
acetic acid in woody plants. Dissertation abstracts, vol. 27B, p.
1772. As cited by USDA (1973).
Fletcher, W.W., 1960. The Effect of Herbicides on Soil Microorganisms.
Blackwell Publishing Ltd. , Great Britain.
Flieg, O., and C. Pfaff, 1951. Movement and decomposition of 2,4-D in
the soil, also it's influence on microbiological transformations.
Lands Forsch 3: 113-22. As cited by USDA (1973).
B-30
Fogels, A., and J.B. Sprague, 1977. Comparative short-term tolerance
of zebrafish, flagfish, and rainbow trout to 5 poisons including
potential reference toxicants. Water Res. 11(9): 811-7. As cited
by Arthur D. Little, Inc. (1979).
Folman, L.C., 1977. Acrolein, Dalapon, Dichlobencil, Diquat, and
Endothal: Bibliography of Toxicity to Aquatic Organisms. U.S.
Fish and Wildlife Service, Fish Pesticide Research Unit, Federal
Center, Denver, CO
Folmar, L.C., H.O. Sanders and A.M. Julin, 1977. Toxicity of the
herbicide glyphosate and several of its formulations to fish and
aquatic invertebrates. Arch. Environ. Contom, Toxicol., 8:
269-78.
Food Protection Committee (1959). See Hodge et al. (1966)
bibliography. As cited by lARC Working Group (1974); (Food
Protection Committee, 1959, not included in bibliography).
Foster, R.K., and R.B. Mckercher, 1973. Laboratory incubation
studies of chlorophenoxyacetic acids in chernozemic soils. Soil
Biol. Biochem. 5: 333-7. As cited by NRCC (1978).
Fowler, H.W. Jr. 1980. Special review of data requirements for 2,4-D.
Internal EPA memorandum to Deputy Assistant Administrator for
Pesticide Programs. June 17.
Foy, D.L. and D. Penner, 1965. Effect of inhibitors and herbicides on
tricarboxycylic acid cycle substrata oxidation by isolated cucumber
mitochondria. Weeds, 13: 226-31.
Frank, R. (1970-1974). Annual Report - Analysis of Samples Connected
with Herbicide Damage Investigations. Provencial Pesticide Residue
Testing Laboratory, Ontario Ministry of Agriculture and Food,
Guelph, Ontario. As cited by NRCC (1978).
B-31
Frank, R. , H.E. Braun, M. Holdrinet, G.J. Sirons, and B.D. Ripley,
1978. Monitoring stream water for pesticides in eleven agricultural
watersheds in southern Ontario, Canada, 1974-77. (Project 4).
International Joint Commission Technical Report (In Preparation).
As cited by NRCC (1978).
Frank, P. A. and R.D. Comes, 1967. Herbicidal residues in pond water
and hydrosoil. Weeds 15: 210-3. As cited by NRCC (1978).
Frank, P. A. and B.H. Grigsby, 1957. Effects of herbicidal sprays on
nitrate accumulation in certain weed species. Weeds 4: 206. As
cited by USDA (1973).
Frank, R., G.J. Sirons, R.A. Campbell, and D. Mewett, 1983.
Residues of 2,4-D, dichlorprop, and picloram in wildberries from
treated rights-of-way and conifer release sites in Ontario, Canada
J. Plant Sci. 63: 195-209.
Freed, V.H. and W.R. Furtick, 1961. The persistance of amitrole in
soil when used for chemical fallow. Hormolog 3(1). As cited by
USDA (1973).
Freed, V.H., and M.L. Montgomery, 1963. The metabolism of
herbicides by plants and soils. Residue Rev. 3: 1-18. As cited
by USDA (1973).
Freeze, R.A., and J. A. Cherry, 1979. Groundwater Prentice-Hall,
Inc., Englewood Cliffs, New Jersey, 604 pp.
Fregly, M.J. and L.B. Kier. 1966. Effect of some substituted sulfamic
acid compounds on development of renal hypertension in rats.
Toxicology and Applied Pharmocology 9:124-38.
Friesen, H.A., 1965. The movement and persistence of dicamba in
soils. Weeds 13: 30-3. As cited by EPA (1975).
B-32
Frissel, M.J., 1961. The adsorption of some organic compounds,
especially herbicides on clay minerals. Verslagen van
Landboukundige on Derzoekingen, nr. 67., Wageningen. 54 pp.
As cited by NRCC (1978).
Frissel, M.J. and G.H. Bolt, 1962. Interaction between certain
ionizable organic compounds (herbicides) and clay minerals. Soil
Sci. 94: 284-91. As cited by NRCC (1978).
Funderburk, H.H., Jr., N.S. Negi, and J.M. Lawrence, 1966.
Photochemical decomposition of diquat and paraquat. Weeds 14:
240, As cited by Simsiman, et al. (1976).
Gangstad, E.O. 1982. Weed Control Methods for Rights-of-Way
Management. CRC Press, Boca Raton, Florida.
Gardiner, J. A. 1975. Substituted uracil herbicides. In: Kearney, P.C.
and D.D. Kaufman, ed. , Herbicides: Chemistry , Degradation, and
mode of Action, 2nd ed. , Volume 11, Marcel Dekkar, Inc.,
pp. 293-321.
Gardiner, J. A., R.W. Reiser, and H. Sherman. 1969. Identification of
the metabolites of bromacil in rat urine. J. Agric. Food Chem.
17(5):967-73.
Gardiner, J. A., R.C. Rhodes, J.B. Adams, Jr., and E.J. Soboczenski.
1969. Synthesis and studies with 2-C-14 labeled bromacil and
terbacil. J. Agr. Food Chem. 17(5): 980-6. As cited by Hill
(1971).
Gaur, A.C., and K.C. Misra, 1972. Effect of 2,4-D on the growth of
Rhizobium Spp. in vitro. Indian J. Microbiol., 12:45-6.
Geissbuhler, H., C. Haselbach, H. Aebi, and L. Ebner. 1963. The
fate of N'-(4-chlorophenoxy)-phenyl-N,N-dimethylurea (C-1983) in
soils and plants. Weed Res. 3:277-97.
B-33
Geissbuhler, H., H. Martin, and G. Voss, 1975. The substituted areas
In; Kearney, P.C. and D.D. Kaufman, eds.. Herbicides:
Chemistry, Degradation, and Mode of Action. Vol.1., pp. 209-91.
As cited by Reed (1982).
Centner, W.A., 1964. Weeds 12: 239. As cited by TRW (1981), no
title provided.
Gesme, J., E. Albanese, A.J. Marias, 1977. Report to Ciba-Geigy
Corporation: Carcinogenicity Study with CGA-24705 Technical in
Albino Mice: IBT No. 622-07925 (8532-07925). CDL: 96719-A;
Unpublished study prepared by Industrial Bio-Test Laboratories,
Inc. for Ciba-Geigy Corp., Greensboro, NC. As cited by EPA
(1980).
Gilderhus, P. A., 1967. Effects of diquat on bluegills and their food
organisms. Progressive Fish-Culturist 29: 67. As cited by
Simsiman, et al. (1976).
Glass, B.L., and W.M. Edwards, 1974. Picloram in lysimeter runoff
and percolation water. Bull. Environ. Contam. Toxicol. 11(2):
109-12 Feb. As cited by Arthur D. Little, Inc. (1979).
Goode. J. 1980. Goldenrods: nuggets in the fall garden. Horticulture
58:21-3.
Goodland, R. 1973. Ecological perspectives of powerlines. In
Goodland, R, ed. Power Lines and the Environment. Prov. of the
CoUoquim, "Biotic Management along Power Transmission
Rights-of-Way" held at the American Institute of Biological Sciences
annual meeting, Amherst, MA. June 21.
Gopalan, H.N.B. and G.D.E. Njagi. 1981. Mutagenicity testing of
pesticides III. Drosophila: Recessive sex-linked Tethals. Abstract
Genetics 97:s44.
B-34
Goring, C.A.I. , and J.W. Hamaker, 1971. The degradation and move-
ment of picloram in soil and water. Down to Earth 27(1): 12-5.
As cited by USDA (1973).
Goring, C.A.I. , C.R. Youngson, and J.W. Hamaker, 1965. Tordon
herbicide ... Disappearance from Soils. Down to Earth 20: 3-5.
As cited by NRCC (1974). Arthur D. Little, Inc. (1979).
Goring, C.A.I. , J.D. Griffith, F.C. O'Melia, H.H. Scott, and C.R.
Youngson, 1967. The effect of Tordon on microorganisms and soil
biological processes. Down to Earth 22(4): 14-7. As cited by
USDA (1973).
Graff, G.L.A., C. Gueuning, and B. Vanderkelen, 1972. Influence de
I'acide 2,4-dichlorophenoxyacetique (2,4-D), un agent myotonisant
sur le m^tabolisme des phosphates acidosolubles des muscles
squelettiques du rat. C.r. Soc. Biol. 166: 1565-8.
Griffith, J.D., 1976. The Effect of Triclopyr on Soil Microorganisms.
Report No. GS-1456. As cited by TRW (1981).
Grisez, T.J. and M. Peace 1973. Requirements for advance
reproduction in Allegheny hardwoods — an interim guide.
U.S.Agric. For. Serv. Res. Note NE-180.
Grossbard, E. and G.F. Wingfield, 1978. Effects of paraquat,
aminotriazole and glyphosate on cellulose decomposition. Weed
Research 18: 347-53.
Grover, R. , 1971. Adsorption of picloram by soil colloids and various
other adsorbents. Weed Sci. 19: 417-8. As cited by TRW (1981).
Grover, R. , 1977. Mobility of dicamba, picloram, and 2,4-D in soil
columns. Weed Sci. 24: 26-8. As cited by NRCC (1978); EPA
(1975).
B-35
Grover, R. and A.E. Smith, 1974. Adsorption studies with the acid
and dimethylamine forms of 2,4-D and dicamba. Can. J. Soil Sci.
54: 179-86. As cited by NRCC (1978).
Gupta, B.N., R.N. Khanna, and K.K. Datta. 1979. Toxicological
studies of ammonium sulfamate in rat after repeated oral
administration. Toxicology 13: 45-9.
Grzenda, A.R., H.P. Nicholson, and W.S. Cox, 1966. Persistence of
four herbicides in pond water. J. Amer. Water Works Assoc. 58:
326. As cited by Simsiman, et al. (1976).
Haagen, A.O. 1953. Ammate in the diet of the deer. The Journal of
Wildlife Management 17(l):33-6.
Haagomes, T. , 1975. DOWCO 233 herbicide - a possible new tool in
vegetation management. Industrial Vegetation Management 7(2):
13-5.
Haas, R.H., C.J. Scifres, M.G. Merkle, R.R. Hahn, and G.O.
Hoffman, 1971. Occurrence and persistence of picloram in
grassland water sources. Weed Res. 11: 54-62. As cited by
NRCC (1974).
Hague, R. and R. Sexton, 1968. Kinetic and equilibrium study of the
adsorption of 2, 4-dichlorophenoxy acetic acid on some surfaces. J.
Colloid Interface Sci. 27: 818-27. As cited by NRCC (1978).
Hallborn, L. and B. Bergman, 1979. Influence of certain herbicides
and a forest fertilizer on the nitrogen fixation by the lichen
Pettigera praetextata oecologia (Berl.) 40: 19-27.
Halter, M.T., 1980. 2,4-D in aquatic environment. In: Literature
Reviews of Four Selected Herbicides: 2,4-D, Dichlorobenil, Diquat
and Endothall. Municipality of Metropolitan Seattle. As cited by
TRW (1981).
B-36
Hamaker, J.W., 1975. Adsorption of Triclopyr in soil. Report No.
GS-1390, February 6. As cited by TRW (1981).
Hamaker, J.W. 1977a. A 45-Day Soil Leaching Test on Triclopyr
(3,5,6-trichloro-2-pyridinyl) Oxyacetic Acid. Report No. GS-1469,
February 7. As cited by TRW (1981).
Hamaker, J.W., 1977b. Photolysis of Triclopyr
(3,5,6-trichloro-2-pyridinyl) oxyacetic acid. Report No. GS-1467,
February 11. As cited by TRW (1981).
Hamaker, J.W. (no date). The Hydrolysis of Triclopyr in Buffered
Distilled Water. Report No. GS-1410. As cited by TRW (1981),
reference no. 29.
Hamaker, J.W., H. Johnston, R.T. Martin, and C.T. Redemann, 1963.
A picolinic acid derivative. A plant growth regulator Science, New
York, pp. 141-363. As cited by USDA (1973).
Hamaker, J.W., C.A.I. Goring, and C.R. Youngson, 1966. Sorption
and leaching of 4-amino-3,5,6-trichloropicolinic acid in soils. Adv.
Chem. Ser. 60: 23-7. As cited by NRCC (1978).
»
Hamaker, J.W., C.R. Youngson, and C.A.I. Goring, 1967. Prediction
of the persistence and activity of Tordon herbicide in soils under
field conditions. Down to Earth 23(2): 30-6. As cited by USDA
(1973).
Hameed, K.M., and C.L. Foy , 1974. Bulletin of the College of Science,
University of Bagdad, Republic of Iraq, vol. 12, part 2. As cited
by TRW (1981).
Hammons, R.H., 1977. Atrazine Persistence in Valentine Loamy Fine
Sand Profile. NTIS, PB-291-497. M.S. Thesis, University of
Nebraska, Lincoln, Nebraska, 55 pp. As cited by TRW (1981).
B-37
14
Han, J. C-Y. 1979a. Residue studies with [ C] fosamine ammonium in
channel catfish. Journal of Toxicology and Environmental Health
5:957-63.
14
Han, J. C-Y. 1979b. Stability of [ C] fosamine ammonium in water
and soils. J. Agric. Food Chem. 27(3) : 564-71. And as cited by
TRW (1981).
Han, J. C-Y. and R.L. Krause. 1979. Microbial activity in soils
treated with fosamine ammonium. Soil Science 128(1) :23-7.
Hance, R.J. 1965a. Observations on the relationship between the
adsorption of diuron and the nature of the adsorbent. Weed Res.
5: 108-14. As cited by Reed (1982).
Hansen, W.H., M.L. Quaife, R.T. Habermann. and O.G. Fitzhugh.
1971. Chronic toxicity of 2 ,4-dichlorophenoxyacetic acid in rats
and dogs. Toxicology and Applied Pharmacology 20:122-9.
Hardell, L. , M. Eriksson and P. Lenner. 1980. Malignant lymphoma
and exposure to chemical substances-especially organic solvents,
chlorophenols and phenoxyacids. Lakairtidningen 77(4) :208-10,
Hardy, T.L., 1966. Effect of Tordon herbicides on aquatic chain
organisms. Down to Earth, 22(2): 11-3.
Harger, T.R., 1975. Soil Dissipation of Dicamba and VEL-4207.
Dissertation, University of Kentucky, Lexington, Kentucky, 93 +
pp. As cited by Velsicol Chemical Corp. (1981).
Harless, R. (Health Effects Research Lab.), 1981. Analyses for di-
and tetra- chlorinated dibenzo-p-dioxins in 2,4-D. Internal EPA
memorandum to M. Dellarco, Dioxin Project Manager, Office of
Toxic Substances, January 16.
B-38
Harris, C.I., 1964. Movement of dicamba and diphenamid in soils.
Weeds 12(2): 112-115. As cited by TRW (1981).
Harris, C.I., 1967. Movement of herbicides in soil. Weeds 15: 214-6.
As cited by Reed (1982); TRW (1981).
Harris, C.I. and G.F. Warren, 1964. Adsorption and desorption of
herbicides by soil. Weeds 12: 120-6. As cited by NRCC (1978).
Harris, C.I., E.A. Woolson, and B.E. Hummer, 1970. Dissipation of
herbicides at three soil depths. Residue Reviews 32: 391-9. As
cited by TRW (1981).
Harvey, John, Jr. (no date available). A Simple Method of Evaluating
Soil Breakdown of C-Pesticides Under Field Conditions.
Unpublished report by E.I. du Pont de Nemours and Co., Inc.,
Wilmington, DE.
Hattan, D.B. 1982. Make Right-of-Way Management Pay! A Proposal of
Forest Management Alternatives to the Present Method of
Vegetation Control for a Section of Interstate 95, Bangor to
Newport, Maine. Manuscript.
Haugen, A.O., 1953. Ammate in the diet of deer. Journal of Wildlife
Management, 17(1): 33-6.
Hawxby, K. et al. , 1977. Effects of various classes of herbicides on 4
species of algae. Pestic. Biochem. Physiol. 7(3): 203-9. As cited
by Arthur D. Little, Inc. (1979).
Heath, R.G., J.W. Spann, E.F. Hill, and J.F. Krietzer, 1972.
Comparative Dietary Toxicities of Pesticides to Birds. Bureau of
Sport Fisheries and Wildlife. Special Scientific Report - Wildlife
No. 152, Washington, D.C. As cited by TRW (1981).
B-39
Hedlund, R.T., 1972. Determination of the Bioconcentration Potential
of 3,5,6-trichloro-2-pyridinol. Report No. GS-1282, November 24.
As cited by TRW (1981).
Hedlund, R.T., and C.R. Youngson, 1972. The rates of
photodecomposition of picloram in aqueous systems. Adv. in
Chem. Ser. Ill: 159-72. As cited by TRW (1981).
Helling, C.S., 1970. Movement of s-triazines in soils. Residue Review
32: 175-210. As cited by Reed (1982).
Helling, C.S., 1971a. Pesticide mobility in soils. I. Parameters of
thin-layer chromatography. Proc. Soil. Sci. Soc. Am. 35: 732-7.
As cited by NRCC (1978); Majke (1976).
Helling, C.S., 1971b. Pesticide mobility in soils II. Applications of
soil thin-layer chromatography. Proc. Soil Sci. , Soc. Am. 35:
737-43. As cited by NRCC (1978); Majke (1976); TRW (1981).
Helling, C.S., 1971c. Pesticide mobility in soils III. Influence of soil
properties. Proc. Soil. Sci. Soc. Am. 35: 743-8. As cited by
NRCC (1978); Majke (1976).
Helling, C.S. and B.C. Turner, 1968. Pesticide mobility:
Determination by soil thin-layer chromatography. Science 162:
562-3. As cited by NRCC (1978).
Hernandez, T.P. and G.F. Warren, 1950. Some factors affecting the
rate of inactivation and leaching of 2,4-D in different soils. Proc.
Am. Soc. Hortic. Sci. 56: 287-93. As cited by NRCC (1978),
USDA (1973).
Herr, D.E., E.W. Stroube, and D.A. Ray, 1966. The movement and
persistence of picloram in soil. Weeds 14: 248-50. As cited by
TRW (1981); NRCC (1974).
B-40
Hilbig, v., K. Lucas and V. Sebek, 1976. Studies of the determination
of toxic effects of derivitives of 2,4-D and 2,4,5-T on incubated
pheasant, quail and hen eggs. 1st report. Anz . Schadlingske. ,
Pflanzenschutz-Ummelschutz. , 49: 21-25.
Hilbig, v., K. Lucas, V. Sebek and H. Munchow, 1976. Studies of the
determination of toxic effects of derivities of 2,4-D and 2,4,5-T on
incubated pheasant, quail and hen eggs. 2nd report. Anz.
Schadlinske, Pflanzenschutz-Umwelschutz. , 49: 65-8.
Hill, E.F., R.G. Health, J.W. Spann, and J.D. Williams. 1975. Lethal
Dietary Toxicities of Environmental Pollutants to Birds. Patuxent
Wildlife Research Center, Laurel, MD. Special Science
Report-Wildlife No. 191. Washington, DC.
Hill, G.D., 1971. Characteristics of Herbicides by Chemical Groups: I.
Substituted Ureas, II. "Hyvar" X Bromacil. Presented at 23rd
Annual California Weed Conference, January 20, 1971, Sacramento,
California. E.I. Du Pont de Nemours Co., Wilmington, DE
Hill, G.D., J.W. McGahen, H.M. Baker, D.W. Finnerty, C.W. Bingeman
1955. The fate of substituted urea herbicides in agricultursd soils.
Agronomy Journal 47(2) :93-124.
Hill, R. , Z. Rollen, D. Renate, L. Needham, 1981. Arch, of Env.
Health 36(1): 11-4. As cited by MACC (1982) no title provided.
Hiltribran, R.C., 1967. Effects of some herbicides on fertilized fish
eggs and fry. Trans. Am. Fish Soc. 96: 414-6. As cited by TRW
(1981) Simsiman et al. (1976).
Hiltibran, R.C., D.L. Underwood and J.S. Fickle, 1972. Fate of
diquat in the aquatic environment. Report No. 52. Water
Resources Center, University of Illinois, Urbana, Illinois. As
cited by Simsiman, et al. , (1976).
B-41
Hinckley, 1972. As cited by Arthur D. Little, Inc. (1979); not
included in bibliography.
Hirota, N. and G.M. Williams. 1979. Persistence and growth of rat
liver neoplastic nodules following cessation of carcinogen exposure.
J. Natl. Cancer Inst. 63(3) : 1257-65.
Hodge, H.C., and E.A. Maynard, W.L. Downs, J.K. Ashton, and L.L.
Salerno, 1966. Tests on mice for evaluating carcinogenicity.
Toxicol. Appl. Pharmacol. 9: 583-96. As cited by lARC Working
Group (1974).
Hodge, H.C., W.L. Downs, B.S. Panner, D.W. Smith, E.A. Maynard,
J.W. Clayton, Jr., and R.C. Rhodes. 1967. Oral toxicity and
metabolism of diuron (N-(3,4-dichlorophenyl) -N', N' -dimethyl-
urea) in rats and dogs. Ed. Cosmet. Toxicol. 5:513-31.
HoUings worth, E.B., 1955. Cotton response to two substituted ureas
and CIPC and their persistence in soil. Proc. South. Weed Sci.
Soc. 8: 294-304. As cited by Reed (1982).
Horsley, S.B. 1977a. Allelopathic inhibition of black cherry by fern,
grass goldenrod, and aster. Can. J. For. Res. 7:205-16.
Horsley, S.B. 1977b. Allelopathic inhibition of black cherry. II.
Inhibition by woodland grass, ferns, and club moss. Can. J. For.
Res. 7:515-9.
Horsley, S.B. and D.A. Marquis 1983. Interference by weeds and deer
with Allegheny hardwood reproduction. Can. J. For. Res.
13:61-9.
House, W.B., et al. , 1967. Assessment of Ecological Effects of
Extensive or Repeated Use of Herbicides. Midwest Research
Institute, Kansas City, Missouri, MRI Project No. 31, pp. 177-85.
As cited by TRW (1981).
B-42
Houseworth, L.D., 1973. Report on Parent Leaching Studies for
CGA-24705: Report No. 1 Received Sep. 26, 1974 under 5G1553.
CDL: 94222-E, Unpublished Study prepared by University of
Missouri-Columbia, Department of Plant Pathology for Ciba-Geigy
Corp., Greensboro, N.C. As cited by EPA (1980).
Howe, D.L.T,, and N. Wright, 1965. The toxicity of paraquat and
diquat. Proc. New Zealand Weed and Pest Cont. 18: 105. As
cited by Simsiman, et al. (1976).
Hsia, M.-T. S., F.V.Z. Bairstow., L.C.T. Shih, J.G. Pounds, and
J.R. Allen. 1977. 3,4,3' ,4'-tetrachloroazobenzene: A potential
environmental toxicant. Research communications in Chemical
Pathology and Pharmacology 17(2) :225-35.
Hughes, J.S. and J.T. Davis, 1963. Variations in toxicity to bluegill
sunfish of phenoxy herbicides. Weeds, 11: 50-3.
Hunter, J.H., and E.H. Stobbe, 1972. Movement and persistence of
picloram in soil. Weed Science 20: 486-9. As cited by TRW (1981).
lARC Working Group. 1974. Evaluation of the Carcinogenic Risk of
Chemicals to Man: Some anti-thyroid and related substances,
nitrofurans and industrial chemicals. Monograph, v. 7., pp. 31-43.
Ingle, L. , 1912. Acute Toxicity of Dimethylamine Salt of 2-methoxy-3,
6-dichlorobenzoic Acid, Banvel D,, Univ. of Illinois, April 26.
Submitted by Velsicol Chemical Corp., June 30, 1965. As cited by
TRW (1981).
Innes, J.R.M., B.M. Ulland, M.G. Valerio, L. Petrucelli, L. Fishbein,
E.R.Hart, A.J. Pallotta, R.R. Bates, M.L. Falk, J.J.Gart, M.
Klein, I. Mitchell, and J. Peters. 1969. Bioassay of pesticides and
industrial chemicals for tumorigenicity in mice: A preliminary note
J. Nat. Cancer Inst. 42:1101-14.
B-43
Inoue K. , Y. Katoh and S. Takayama 1981. In vitro transformation
of hamster embryo cells by 3-(N-salicyloyl) amino-l,2,4-triazole.
Toxicology Letters 7:211-5.
Isensee, A.R., 1971. Biomagnification Study of 2,4,5-T. Information
supplied to the panel by E. Kenaga, March 17, 1977. As cited by
NRCC (1978).
Isensee, A. R. , and G. Jones, 1977. Absorption and translocation of
root and foliage applied 2 ,4-dichlorophenol, 2,7-dichlorodibenzo-p-
dioxin, and 2, 3,7,8-tetrachlorodibenzo-p-dioxin, J. Agr. Fd,
Chem., 19: 1210-4.
Ivey, M.J. and H. Andrews, 1965. Leaching of simazine, atrazine,
diuron, and DCPA in soil columns. Proc. South. Weed Sci. Soc.
18: 670. As cited by Reed (1982).
Johansen, C.A., 1959. Bee poisoning. A hazard of applying
agricultural chemicals. Washington State Coll. Agr. Expt, Sta.
Circ. No. 356. As cited by USDA (1973).
Johansen, C.A. , 1980. Letter regarding pesticide toxicity to bees.
Washington State University, Department of Entomology, Pullman,
Washington, May 12, 1980. As cited by TRW (1981).
Johnson, J.E. 1971. The public health implications of widespread use
of phenoxy herbicides and picloram. Bioscience. 21(17)899-905.
Johnson, D.R. and R.M. Hansen, 1969. Effects of range treatments
with 2,4-D on rodent populations. J. Wildlife Management, 33:
125-32.
JoUiffe, V.A., B.E. Day, L.S. Jordan, and J.D. Mann., 1967. Method
of determining bromacil in soils and plant tissues. J. Agric. Food
Chem. 17: 174-7. As cited by HiU (1971).
B-44
Jones, R.O. Tolerance of the fry of common warm-water fishes to some
chemicals employed by fish culture. Proc. 16th Ann. Conf.
Southeast Assoc. Game Fish Comm. pp. 436-45. As cited by TRW
(1981).
Jorgensen, N. 1978. A Sierra Club Naturalist's Guide to Southern New
England. Sierra Club Books, San Francisco, CA.
Jorgenson, T.A., C.J. Rushbrook, and G.W. Newell. 1976. In vivo
mutagenesis investigations of ten commercial pesticides. Abstract
no. 41. Topxicol. Appl. Pharmacol. 37:109.
Jukes, T.H. and C.B. Shafter, 1960. Antithyroid effects of
aminotriazole. Science, 132: 296-7.
Kartesz, J.T. and R. Kartesz, 1980. A Synonymized Checklist of the
Vascular Flora of the United States, Canada and Greenland.
University North Carolina Press, Chapel Hill.
Kasza, Louis. 1980. Review of liver slides from National Cancer
Institute picloram experiment. Internal EPA memorandum to Robert
J. Taylor, Registration Division, May 1.
Kaufman, D.D., and J. Blake, 1970. Degradation of atrazine by soil
fungi. Soil Biol. Biochem. 2: 73-80. As cited by TRW (1981).
\
Kaufman, D.D., et al. , 1968. Chemical versus microbial decomposition
of amitrole in soil. Weed Science 16(2): 266-72. As cited by TRW
(1981).
Kearney, P.C., 1966. Metabolism of herbicides in soils. Adv. Chem.
Ser. 60: 250-62. As cited by NRCC (1978).
Kearney, P.C. and D.D. Kaufman, 1975. Degradation of Herbicides,
vols. 1 and 2. Maul Dekker, Inc., New York, NY.
B-45
Kearney, P.C. et al. , 1977. Distribution, Movement, Persistence, and
Metabolism of N-nitrosoatrazine in soils: A model aquatic
ecosystem. J. Agric. Food. Chem. 25(5): 177-81. As cited by
TRW (1981).
Kenaga, E.E., 1969. Tordon herbicides -evaluation of safety to fish and
birds. Down to Earth, 25(1): 5-9.
Kennedy, G.L., 1976. Letter [dated Dec. 13, 1976, interim report on
IBT No. 8531-07926, 2 year chronic toxicity of CGA24705 in albino
rats] to George Rolofson. CDL: 95768-D. Unpublished study
prepared by Industrial Bio-Test Laboratory, Inc. for Ciba-Geigy
Corp., Greensboro, N.C. As cited by EPA (1980).
Khalatkar, A.S. and Y.R. Bhargava 1982. 2,4-Dichlorophenoxyacetic
acid-A new environmental mutagen Mutation Research 103:111-4.
Khan, S.U., 1972. Interaction of humic acid with chlorinated
phenoxyacetic acid and benzoic acid. Environ. Letters 4: 141-8.
As cited by NRCC (1974).
Khan, S.U., 1973. Equilibrium and kinetic studies of the adsorption of
2,4-D and picloram on humic acid. Can. J. Soil Sci. 53: 429-34.
As cited by NRCC (1978), EPA (1975).
Khan, S.U., 1973. Interaction of humic substances with bipyridylium
herbicides. Can. J. Soil. Sci. 53: 199. As cited by Simsiman, et
al. (1976).
14
Khanna. S., and S.C. Fang , 1966. Metabolism of C-labeled
2, 4-dichlorophenoxy acetic acid in rats. J. of Agric. Food Chem.
14: 500-3. And as cited by USDA (1973).
Khera, K.S. and W.P. McKinley. 1972. Pre-and postnatal studies on
2,4,5-trichlorophenoxyacetic acid, 2,4-dichlorophenoxyacetic acid
B-46
and their derivatives in rats. Toxicology and Applied
Pharmocology 22:14-28.
Khera, K.S. C. Whalen, G. Trivett, and G. Angers. 1979.
Teratogenicity studies on pesticidal formulations of dimethoate,
diuron and lindane in rats. Bull. Environm. Contam. Toxicol.
22:522-9.
Khera, L.S. and J. A. Ruddick. 1973. Polychlorodibenzo-p-dioxins:
Perinatal effects and the dominant lethal test in Wistar rats. Health
Protection Branch Department of National Health and Welfare.
Tunney's Pasture, Ottawa, Ontario, KIA 0L2, Canada
i
Klaasen, H.E., and A.M. Kadoura, 1979. Distribution and retention of
atrazine and carbofuran in farm pond ecosystems. Archives
Environ. Contamin. Toxicology 8: 34-353. As cited by TRW
(1981).
Klingman, G.C., and F.M. Aston, 1975. Weed Science: Principles and
Practice. John Wiley and Sons, New York, New York, 431 pp.
As cited by Reed (1982).
Knight, B.A.C., and T.E. Tolimson, 1967. The interaction of paraquat
(1: 1' dimethyl 4: 4'-dipyridylium dichloride) with mineral soils. J.
Soil Sc^ience 18: 238. As cited by Simsiman, et al. (1976).
Konnai, M., Y. Takeuchi, and T. Takematsu, 1974. Ringyoyo josozai
no oojochu niokeru zanryu oyobi ido nikansuru kisoteki kenkyu -
Basic studies on the residues and movements of forestry herbicides
in soil-1 Utsunomiya Daigaku Nogakubu Gakujutsu hokoku.
Bulletin of the College of Agriculture, Utsunomiya University
19(1): 95-112. As cited by EPA (1981a).
Konstantinova, T.K., L.P. Epimenko, and T.A. Antonenko. 1976. The
embryotrophic effect of the dissociation products of herbicides
based on 2,4-D. Giyena I. Sanitariya 11:102-5.
B-47
Kopischke, A.D., 1972. The effect of 2,4-D and diesel fuel on egg
hatchability . Journal of Wildlife Management 26: 1353-6.
Korte, C. and J. Jalal, 1982. 2,4-D induced clastogenicity and
elevated rates of sister chromatid exchanges in cultured human
lymphocytes. J. Hered, 73(3): 224-6.
Kozlova, E.I., A. A. Belousova, and V.S. Vandariera, 1967. Effect of
simazine and atrazine on the development of soil microorganisms.
Agrobiologiya 2: 271-7. As cited by TRW (1981).
Kozlowski, T.T., and J.E. Kuntz, 1973. Effects of simazine, atrazine,
propazine and eptam on growth and development of pine seedlings.
Soil Science 95(3): 164-74, 1973. As cited by TRW (1981).
Krefting, L.W. and H.L. Hansen, 1969. Increasing browse for deer by
aerial applications of 2,4-D. Journal of Wildlife Management 33:
784-90.
Kubinski, H. , G.E. Gutzke and Z.O. Kubinski 1981. DN A- cell-bin ding
(DCB) assay for suspected carcinogens and mutagens. Mutation
Research 89, 95-136.
Kudzina, G.D. and D.I. Golovan, 1972. Comparative
sanitary-toxicological and cell culture evaluation of the
chlorobenzoic acid herbicide group. Abstract. Vrach Delo 1:
125-8. As cited by Arthur D. Little, Inc. (1979).
Laamanen, I., M. Sorsa, D. Banford, U. Gripenberg, and T. Meretoja.
1976. Mutagenicity and toxicity of amitrole. I. Drosophila tests.
Mutation Research 40: 185-90
Lamb, J.C. IV, and J. A. Moore 1981. Development and viability of
offspring of male mice treated with chlorinated phenoxy acids and
2,3,7,8 - tetrachlorodibenzo p-dioxin. Journal of Toxicoloy and
Environmental Health 8: 835-44.
B-48
Landauer, W. and N. Salam. 1972. Aspects of dimethyl sulfoxide as
solvent for teratogens. Developmental Biology 28: 35-46
Landauer, W., N. Salan and D. Sopher. 1971. The herbicide
3-amino-l,2,4-triazole (amitrole) as teratogen. Environmental
Research 4: 539-43
Laskowski, D.A., et al. , 1975. Aerobic Decomposition Rates of
14
C-Triclopyr in Several Soils. Status Report. Report No.
GH-C-863. October 16. As cited by TRW (1981).
Lavy, T.L., F.W. Roeth, and C.R. Fenster, 1963. Degradation of
2-4-D and atrazine at three soils depths in the field. J.
Environmental Quality 2: 132-7. As cited by TRW (1981).
Leistra, M. , J.H. Smelt, and R. Zandvoort, 1975. Persistence and
mobility of bromacil in orchard soils. Weed Res. 15: 243-47. And
as cited by Reed (1982).
Lewis, R.J., Sr. and R.L. Tatken. 1982. Registry of Toxic Effects of
Chemical Substances, 1980 Edition, Volumes land 2. U.S.
Department of Health and Human Services, Washington, D.C.
Lilly Research Laboratories, 1982. Graslan for Rangeland Brush
Control. Unpublished general summary prepared by Lilly Res.
Lab., Greenfield, IN
Lisk, D.J., W.H. Gutenmann, C.A. Bache, R.G. Wagner, and D.G.
Wagner, 1963. Elimination of 2,4-D in the urine of steers fed
4-(-2,4-DB) or 2,4-D. J. Dairy Sci. 46: 1435-6. As cited by
Minnesota Department of Health (1978).
Litchfield, M.H., J.W. Daniel, and S. Longshaw, 1973. The tissue
distribution of the bipyridylium herbicides diquat and paraquat in
rats and mice. Toxicology 1: 155. As cited by Simsiman, et al.
(1976).
B-49
Liu, L.C. and H.R. Cibes-Viade, 1973. Adsorption of fluometuron,
prometryne, sencor, and 2,4-D by soils. Univ. Puerto Rico, J.
Agric. 57: 286-93. As cited by NRCC (1978).
Loktionov, V.N., W.A. Budarkov, A.I. Kuznetsov, and N.V.
Kuznetsova, 1973. Toxicological characteristics of the manufacture
of dichlorophenoxyacetic acid. Veterinariya (Moscow) 5: 107-9.
As cited by NRCC (1978).
Loos, M.A., 1969. Phenoxyalkanoic acids. In: Kearney, P.C. and
D.D. Kaufman, eds. Degradation of Herbicides, Marcel Dekker,
New York, New York, pp. 1-49. As cited by USDA (1973).
Loos, M.A., R.N. Roberts, and M. Alexander, 1967a. Phenols as
intermediates in the decomposition of phenoxyacetates by an
Arthrobacter species. Canadian Journal of Microbiology 13:
679-90. As cited by USDA (1973).
Loos, M.A., R.N. Roberts, and M. Alexander, 1967b. Formation of
2 , 4-dichlorophenol and 2,4-dichloroanisole from
2 , 4-dichlorophenoxyacetate by Arthrobacter sp. Canadian Journal
of Microbiology 13: 691-9. As cited by USDA (1973).
Loprieno, N., R. Barale, L. Marigni, S. Presciuttini, A.M. Rossi, I.
Sbrana L. , Zaccaro, A. Abbondandolo, and S. Bonatti. 1980.
Results of mutagenicity tests on the herbicide atrazine. Abstract.
Mutation Research 74(3): 250.
Lorz , H.W., et al. , 1979. Effects of Selected Herbicides on Sraolting of
Coho Salmon. EPA, Washington, D.C. As cited by USDOE
(1980).
Lowe, 1964. As cited by NRCC (1978), no citation provided.
B-50
Ludzack, F.J. and J.W. Mandia. Behavior of 3-amino-l,2,4-triazole in
surface water and sewage treatment. Purdue University Engr.
Bull, Ext. Series No. 109. As cited by TRW (1981).
Lusby, A.F., Z. Simmons, and P.M. McGuire 1979. Variation in
mutagenicity of s-triazine compounds tested on four Salmonella
strains. Environmental Mutagenesis 1: 287-90.
Lutz-Ostertag , Y. and Lutz , M.H., 1970. Action nefaste de I'herbicide
2,4-D sur le development embryonnaire et al fecondite du gibier a
plumes. C.r. Acad. Sci. Ser. D. 271: 2418-21. As cited by
NRCC (1978).
Lynn, G.E., 1965. A review of toxicological information on Tordon
herbicides. Down to Earth, 20(4): 6-8.
Lynn, G.E. and R.C. Barrons, 1952. The hydrocyanic (HCN) content
of wild cherry leaves sprayed with a brush killer containing low
volatile esters of 2,4-D and 2,4,5-T. Proc. 6th NE. Weed Control
Conf. p. 331. As cited by USDA (1973).
MACC, 1982. The Impacts of Chemical Herbicides, Tufts University,
Medford, MA
;
V,
Magee, L.A. and A.R. Colmar, 1956. Some effects of
2,4-dichlorophenoxyacetic acid upon Azotobacter as measured by
respiration inhibition. Weeds 4: 124-30. As cited by NRCC
(1978).
Maier-Bode, H., 1973. Residues and side effects of herbicides in
Forest Protection. Anz. Schaedlingsk Pflanzen-Umeltschung ,
46(2): 17-24.
Majka, J.T., 1976. Adsorption, Mobility and Degradation of Cyanazine
and Diuron in Soils. Thesis. Nebraska Univ. Prepared by Office
B-51
of Water Research and Technology, Washington, D.C. January
1976.
Maki, S. 1973. Agricultural Chemicals and Toxicity Series #5. Bulletin
of Forestry Experiment Station (Japan) 44: 11-4
Malina, M.A., 1973. Dicamba. Anal. Methods Pestic. Plant Growth
Regul. 7: 545-67.
Manigold, D.B. and J. A. Schulze, 1969. Pesticides in selected western
streams, a progress report. Pestic Monit. J. 3: 124-35. As cited
by NRCC (1978).
Manzo, L. , C. Gregotti, A. DiNucci, and P. Richelrai, 1979.
Toxicology of paraquat and related bipyridyls: Biochemical,
clinical and therapeutic aspects. Pesticide and Toxic Chemical
News 7(37): 404-10.
Marriage, P.B. et al, 1975. Residues of atrazine, simazine, linuron,
and diuron after repeated annual applications in a peach orchard.
Weed Res. 15: 377-9. As cited by TRW (1981).
Marston, R.B., D.W. Schultz, T. Shiroyama, and L.V. Snyder, 1968.
Pesticides in water: amitrole concentrations in creek waters
downstream from an aerially sprayed watershed sub-basin. Pest.
Mont. J. 2(3): 123-8. As cited by TRW (1981); USDA (1973).
McCall, H.G., R.W. Bovey, M.G. McCully, and M.G. Merkle, 1972.
Adsorption and desorption of picloram, trifluralin, and paraquat by
ionic and non-ionic exchange resins. Weed Science 20: 250-5. As
cited by TRW (1981).
McClure, G.W., 1970. Accelerated degradation of herbicides in soil by
the application of microbial nutrient broths. Contrib . Boyce
Thompson Inst. 24(11): 235-40. As cited by Velsicol Chemical
Corp. (1981).
B-52
McCoUister, D.D. and M.F, Leng, 1969. Toxicology of picloram and
safety evaluation of Tordon herbicides. Down to Earch, 25(2):
5-10.
McCormick, L.L., and A.E. Hiltbold, 1966. Microbial decomposition of
atrazine and diuron in soil. Weeds 14: 77-166. As cited by TRW
(1981).
McGahen, J.W. and G.E. Hoffmann 1966. Absence of mutagenic effects
of 3-and 6-alkyl -5- bromouracil herbicides on a bacteriophage.
Nature 5029: 1241-2
McGahen, L.L. and J.M. Tiedje, 1978. Metabolism of two new
acytanilide herbicides, Antor Herbicide (H-22234) and Dual
(Metolachlor) by the soil fungus Chaetomium globosum. Journal of
Agricultural Food Chemistry 26(2): 414-9. As cited by EPA
(1980).
McGee, C.E. and R.C. Smith 1967. Undisturbed rhododendron thickets
are not spreading. J. For. 65: 334-5
Mckellar, R.L., 1977. Residues of Triclopyr, 3,5,6-Trichloro-2-
pyridinol, and 2-Methoxy-3,5,6-trichloropyridine in Soil Treated
with Garlon 3A Herbicide. Report No. GH-C-983, April 11. As
cited by TRW (1981).
McLaughlin, R.M., 1951. Toxicity of herbicides. Proc. Northeast Weed
Control Conf. 5: 3-4. As cited by NRCC (1978).
Meadows, M.W. and O. Smith, 1949. Effect of temperature, organic
matter, pH and rates of application of persistence of 2,4-D in soil.
Proc. Northeast Weed Control Conf. 3: 24-9. As cited by NRCC
(1978).
Meikle, R.W, C.R. Youngson, R.T. Hedlund, C.A.I. Goring, and W.W.
Addington, 1973. Decomposition of picloram by soil
B-53
microorganisms: A proposed reaction sequence. Submitted to
Weed Science, May 1973. As cited by NRCC (1974).
Meikle, R.W., et al, 1974. Decomposition of picloram by soil
microorganisms. A proposed reaction sequence. Weed Science 22:
263-8. As cited by TRW (1981).
Mensik, D.C., R.V. Johnston, M.N. Pinkerton and E.B. Whorton, Jr.
(no date available) . The Cytogenetic Effects of Picloram on the
Bone Marrow Cells of Rats. Unpublished report by Dow Chemical
USA, Freeport, TX.
Meretoja, T., U. Gripenberg, D. Banford, I. Loananen, and M. Sorsa
1976. Mutagenicity and toxicity of amitrole.II. Human lymphocyte
culture tests. Mutation Research 40: 191-6.
Merkle, M.G., R.W, Bovey, and F.S. Davis, 1967. Factors affecting
the persistence of picloram in soil. Agron J. 59: 413-5. As cited
by TRW (1981).
Metcalf, R.L. and J.R. Sanborn, 1975. Pesticides and environmental
quality in Illinois. 111. Nat. Hist. Surv. Bull. 31: 381-435. As
cited by NRCC (1978).
Milkowska, A. and A. Gorzelak, 1966. Effect of atrazine and simazine
on the soil microflora in weed control in forest nurseries. Sylvan
110(11): 13-22.
Miller, J.H., P.E. Keeley, R.J. Thullen, and C.H. Carter, 1977.
Persistence and movement of ten herbicides in soil. Weed Sci. 26:
20-7. As cited by Reed (1982).
Miller, O.K., Jr., 1972. Mushrooms of North America, E.P. Duttan and
Co., Inc., New York, New York.
B-54
Mills and J.I. Lowe. (Gulf-breeze Lab Unpublished data [a]) Toxicity
of herbicides to estaurine animals. Pesticide Petition #8F0725. As
cited by EPA (1975), reference no. 6 in Section VI.
Mills and J.I. Lowe. (Gulf-breeze Lab Unpublished data [b]). As
cited by EPA (1975) reference no. 10 in Section VI.
Minnesota Department of Health 1978. Assessment of Human Health Risk
Associated with the Use of 2,4-D in Forestry Management,
Minneapolis, MN.
Mitchell, B., 1969. Persistence of picloram residues. Farm Research
News 10(1): 16. As cited by TRW (1981).
Mitchell, J.W., R.E. Hodgson, and C.F. Gaetjens, 1946. Tolerance of
farm animals to feed contaminated by 2,4-D. J. Anim. Sci. 5:
226. As cited by Gangstad (1982).
Moffett, J.O., 1972. Toxicity of some herbicidal sprays to honey bees.
J. of Economic Entomology, 65(1): 32-6.
Moffett, J.O. and H.L. Morton, 1975. How herbicides affect
honeybees. Am. Bee J. 115: 178-9, 200. As cited by NRCC
(1978).
Moffett, J.O., H.L. Morton, and R.H. MacDonald, 1972. Toxicity of
some herbicidal sprays to honeybees. J. Econ. Entomol 65: 32-6.
As cited by TRW (1981); NRCC (1978).
Monsanto, 1982 (July). Roundup Herbicide Bulletin, No. 3. Monsanto
Co., St. Louis, MO
Monsanto (no publication date provided [a]). Material Safety Data
Sheet for Roundup Herbicide, Monsanto Co., St. Louis, MO
B-55
Monsanto Company (no publication date provided [a]). Data provided
by Monsanto Agricultural Research Department, St. Louis, MO In:
Environmental Fate File, Glyphosate, U.S. Environmental Protection
Agency. As cited by TRW (1981) reference no. 26 on page A-168.
Moore, D.J., 1976. Practical Alternatives to 2,4,5-T for Chemical
Control of Brush Along Drainage Ditches and General Watershed
Use. PB-262/217-3ST. Office of Water Research and Technology,
Washington, D.C. As cited by TRW (1981).
Moriya, M. , T. Ohta, K. Watanabe, T. Miyazawa, K. Kato and Y.
Shirasu 1983. Further mutagenicity studies on pesticides in
bacterial reversion assay systems. Mutation Research 116:
185-216
Morrow, L.A. and M.K. McCarthy, 1976. Selectivity and soil
persistence of certain herbicides used on perennial forage grasses.
J. Envir. Qual. 5(4): 462-5. As cited by Reed (1982).
Morton, H.L. E.D. Robinson and R.E. Meyer, 1967. Persistance of
2,4-D, 2,4,5-T and dicamba in range forage grasses. Weeds, 15:
268-71.
Morton, H.L., J.O. Moffett, and R.H. MacDonald, 1972. Toxicity of
herbicides to newly emerged honeybees. Environ. Entomol. 1:
102-4. As cited by TRW (1981); USDA (1973).
Mullison, J.W. 1979. Herbicide Handbook of Weed Science Society of
America, 4th edition. Weed Science Society of America, Cham-
paign, IL.
Mullison, W.R. 1981. Public concerns about the herbicide 2,4-D, in
34th Annual Meeting of the Western Society of Weed Science.
Murnik, M.R. 1976. Mutagenicity of widely used herbicides. Abstract.
Genetics. 83: 554.
B-56
Murnik, M.R, and C.L. Nash. 1977. Mutagenicity of the triazine
herbicides atrazine, cyanazine and simazine in Drisophila
melanogaster. Journal of Toxicology and Environmental Health 3:
691-7.
Murray, D.S., W.L. Rieck, and J.Q. Lynd, 1969. Microbial
degradation of five substituted urea herbicides. Weed Sci. 17:
52-5. As cited by Reed (1982).
Mustafa, M.A. and Y. Gamar, 1972. Adsorption and desorption of
diuron as a function of soil properties. Soil Sci. Soc. of Amer.
Proc. 36(4): 561-5. As cited by Reed (1982).
Naishtein, S.Y., G.Y. Chegrinetz, G.F. Voronova, R.G. Nikula and
M.D. Bezborod'ko, 1981. Materials for substantiating the maximum
permissible concentration of a Banvel-D herbicide. Soil. Gig.
Sanit. 1: 86-8. As cited by Vesicol Chemical Corp. (1981).
Napalkov, N.P., 1969. On Blastomogenic Action of Thyreostatic
Substances. lECO USSR Acad. Med. Sci. Moscow, Monograph. As
cited by lARC Working Group (1974).
NCI 1978. ' Bioassay of picloram for possible carcinogenicity.
Carcinogenesis. Technical Report Series No. 23 CAS No.
1918-02-1.
NCI, 1979. Bioassay of 2,7-dichlorodibenzo-p-dioxin (DCDD) for
possible carcinogenicity. Carcinogenesis. Technical Report
Series. No. 123 CAS No. 33857-26-0.
Newell, G.W. and J.V. DiUey, 1978. Teratology and Acute Toxicology
of Selected Chemical Pesticides Administered by Inhalation.
Contract No. 68-02-1751. EPA, Health Effects Research
Laboratory, Research Triangle Park, N.C.
B-57
Newman, J.F., and J.M. Way, 1966. Some ecological observations on
the use of paraquat and diquat as aquatic herbicides. Proc. 8th
Brit. Weed Control Conf. 2: 582. As cited by Simsiman, et al.
(1976).
Newton, M. , 1979. Herbicide and Insecticide Technical Properties and
Herbicide Use Guidelines. Oregon St. University. As cited by
TRW (1981).
Newton, M. and J. A. Norgren, 1977. Silvicultural Chemicals and
Protection of Water Quality. EPA-910/ 9-77-036. U.S. EPA, Region
X, Seattle, WA June 1977, 240 pp. As cited by TRW (1981).
Nham, D. and W.A. Harrison, 1977a. Report to Ciba-Geigy
Corporation: Acute Oral Toxicity Study with Dual 8E in Albino
Rats: IBT No. 8530-10822. CDL: 232191-A. Unpublished study
prepared for Ciba-Geigy Corp., Greensboro, N.C. As cited by
EPA (1980).
Nham, D. and W.A. Harrison, 1977b. Report to Ciba-Geigy
Corporation: Acute Dermal Toxicity Study with Dual 8E in Albino
Rabbits: IBT 8530-10822. CDL: 232191-B, Unpublished study
prepared for Ciba-Geigy Corp., Greensboro, N.C. As cited by
EPA (1980).
Niculescu-Duvaz , I., T. Craescu, M. Tugulea, A. Croisy, and P.C.
Jacquignon. 1981. A quaintitative structure-activity analysis of
the mutagenic and carcinogenic action of 43 structurally related
heterocyclic compounds. Carcinogenesis. 2(4) 269-75.
Niering, W.A. and R.H. Goodwin 1974. Creation of relatively stable
shrublands with herbicides: Arresting "succession" on
rights-of-way and pastureland. Ecology 55:784-95.
Norris, L.A., 1966. Degradation of 2,4-D and 2,4,5-T in forest litter.
J. Forestry 64(7): 475-6. As cited by USDA (1973).
B-58
Norris, L.A., 1967, Chemical brush control and herbicide residues in
the forest environment. In: Herbicides and Vegetation
Management. School of Forestry, Oregon State University,
Corvallis, OR, pp. 103-23. As cited by USDA (1973).
Norris, L.A. , 1969. Herbicide runoff from forest lands sprayed in
summer. Research Progress Report, Western Society of Weed
Science, Las Vegas, pp. 24-6. As cited by TRW (1981).
Norris, L.A., 1970a. Degradation of herbicides in the forest floor.
In: Youngberg, C.T. and C.B. Davey, eds., Tree Growth and
Forest Soils. Oregon State Univ., Corvallis, OR, pp. 397-411.
As cited by TRW (1981).
Norris, L.A., 1970b. The Kinetics of Adsorption and Desorption of
2,4-D, 2,4,5-T, Picloram and Amitrole on Forest Floor material.
Research Progress Report, Western Society of Weed Science, pp.
103-4. As cited by TRW (1981).
Norris, L.A. 1971. Chemical brush control: Assessing the hazard.
Journal of Forestry 69(10): 715-20. As cited by TRW (1981).
Norris, L.A,;>, 1971a. The Behavior of Herbicides in the Forest. U.S.
Forest Service, Pacific N.W. Forest and Range Experiment Station,
Mimeo 24 pp. As cited by USDA (1973).
Norris, L.A., 1976. Behavior and impact of some herbicides in the
forest. In Byrnes, W.R. and H.R. Holt, eds.. Herbicides in the
Forest (Proc. John S. Wright For. Conf.) Purdue Univ., Dept.
For Nat. Resources, West Lafayette, IN
Norris, L.A., and M.L. Montgomery, 1975. Dicamba residues in
streams after forest spraying. Bull. Environ. Contam. Toxicol.
13(1): 1-8. As cited by TRW (1981).
B-59
Norris, L.A., and D.G. Moore, 1971. The entry and fate of forest
chemicals in streams. In: Proceeding of a Short Course for
Herbicide Applicators, Oregon State University, Corvallis, OR. As
cited by USDOE (1980).
Norris, L.A., N. Newton, and J. Zavitkavoski, 1967. Stream
contamination with amitrole from forest spray operations. West
Weed Contr. Conf. Res. Prog. Rpt. , pp. 33-5. As cited by USDA
(1973).
Norris, L.A., M.L. Montgomery, and G.D. Savelle, 1976. Behavior of
triclopyr (DOWCO 233) in soil and stream water on a small
watershed, southwest Oregon. Presented at Weed Science Society
Meeting, 1976 Annual Meeting, Denver, CO As cited by TRW
(1981)
Norris, L.A., M.L. Montgomery, and J. Warren, 1976a. Leaching and
persistence characteristics of picloram and 2,4-D on a small
watershed in southwest Oregon. Abstract 81. Abstracts, 1976
meeting of the Weed Science Society of America. Feb, 3-5.
Denver, Colorado. As cited by TRW (1981).
Norris, L.A., et al. , 1977. The fate of picloram, 2,4-D, and triclopyr
in small hillside pastures in southwest Oregon. Abstract of Annual
Meeting of American Society of Range Management, pp. 25-6. As
cited by TRW (1981).
Northeastern Regional Pesticide Coordinators, 1974. Pesticide
Applicator Training Manual, Core Manual, Cooperative Extension
Service, Amherst, MA.
Norton, T.R., 1975. Metabolism of toxic substances. In: Casarett,
L.J. and J. Doull, eds.. Toxicology - The Basic Science of
Poisons, MacMillan Publishing Co., Inc., New York, New York As
cited by TRW (1981).
B-60
NRCC, 1974. Picloram: The Effects of its Use as a Herbicide on
Environmental Quality. National Research Council of Canada, No.
13684. As cited by TRW (1981); USDOE (1980).
NRCC. 1978. Phenoxy Herbicides - Their Effects on Environmental
Quality. National Research Council Canada No. 16075. Ottawa
Canada.
Nutman, P.S., H.G. Thornton, and J.H. Quastel, 1945. Inhibition of
plant-growth by 2, 4-dichlorphenoxy acetic acid and other
plant-growth substances. Nature 155: 498-500. As cited by
NRCC (1978).
O' Conner, G.A. and J.U. Anderson, 1974. Soil factors affecting the
adsorption of 2,4,5-T. Proc. Soil Sci. Soc. Am. 38: 433-6. As
cited by NRCC (1978).
Odum, E.P. 1969. The strategy of ecosystem development. Science
164:262-70.
Ogle, R.E. and G.F. Warren, 1954. Fate and activity of herbicides in
soils. Weeds 3: 257-73. As cited by NRCC (1978).
OSHA. 1980. Identification, classification and regulation of potential
occupational carcinogens. Federal Register 45(15), January 22.
Ouellette, R.P. and J. A. King, 1977. Chemical Pesticides Register.
McGraw-Hill Book Company, New York, New York.
Palmer, J.S. and Radeleff, R.D., 1969. The Toxicity of Some Organic
Herbicides to Cattle, Sheep, and Chickens. Product Res. Rep.
No. 106, Agricultural Research Service, U.S. Dept. of
Agriculture, Washington, D.C. As cited by Gangsted (1982); TRW
(1981).
B-61
Pasi, A., J.W. Embree, Jr., G.H. Eisenlord and C.H. Hine. 1974.
Assessment of the mutagenic properties of diquat and paraquat in
the murine dominant lethal test. Mutation Research 26:171-5.
Peck, D.E., D.L. Corwin, and W.J. Farmer, 1980.
Adsorption-desorption of diuron by freshwater sediments. J.
Environ. Qual. 9(1): 101-6
Pemberton, J.M. 1979. Pesticide degrading plasmids: A biological
answer to environmental pollution by phenoxy herbicides. Ambio
8(5): 202-5.
Peruich, J. A. and J.L. Lockwood, 1978. Interaction of atrazine with
soil microorganisms. Population changes and accumulation. Can.
J. of Microbiol. 24: 1145-52.
Peters, J.W. and R.M. Wok. 1973. Effects of atrazine on reproduction
in rats. Bulletin of Environmental Contamination and Toxicology
9(5):301-4.
Petrides, G.A. 1972. A Field Guide to Trees and Shrubs. Second
edition. The Peterson Field Guild Series, Houghton Mifflin Co.,
Boston, MA.
Phillip, W.M., and K.C. Feltner, 1972. Persistence and movement of
picloram in two Kansas soils. Weed Science 20: 110-6, As cited
by NRCC (1974).
Pilinskaya, M.A. 1974. Cytogenetic effect of the herbicide 2,4-D on
human and animal chromosomes. Tgitologiya i. Genetika 8(3):202-6.
Pimentel, D., 1971. Ecological Effects of Pesticides on Non-Target
Species. Supt. Docs. GPO 4106-0029 Executive Office of the
President, Office of Science and Technology Report, U.S.
Government Printing Office, Washington, D.C. 220 p. June, 1971.
As cited by TRW (1981), Arthur D. Little, Inc. (1979).
B-62
Pipe, A. and D. Cullimore, 1980. Bull, of Env. Contam. Tox. 24:
306-12. As cited by MACC (1982).
Plewa, M.J. 1978. Activation of Chemicals into mutagens by green
plants: A preliminary discussion. Environmental Health
Perspectives 27:45-50.
Plewa, M.J. and J.M. Gentile. 1976. Mutagenicity of Atrazine: A
maize-microbe bioassay. Mutation Research 38:287-292.
Plimmer, J.R., et al. , 1967. Amitrole decomposition by free-radical
generating systems and by soils. J. Agric. Food Chem. 15(6).
As cited by TRW (1981).
Pohlheim, E. and G. Gunther. 1977. Mutagenicity testing of herbicides
with a naploid Pelargonium. Abstract no. 61. Mutation Research
46:232.
Pons, R. and M. Pussard, 1980. Abstract from ACTA Oecol. Appl.
1(1): 15-20. As cited by MACC (1982).
Poole, D.C., V.F. Simmon and G.W. Newell, 1977. In vitro mutagenic
activity of fourteen pesticides. Toxicol. Appl. Pharamcol. , 41(1):
196-7.
Portmann, J.E., and K.E. Wilson, 1971. The Toxicity of 140
Substances to the Brown Shrimp and Other Marine Animals.
Shellfish Information Leaflet No. 22. Ministry of Agriculture,
Fisheries and Food Fisheries Laboratory, Burnham-on-Crouch,
Essex, England. As cited by Simsiman, et al. (1976).
Pound, C.E. and F.E. Egler. 1953. Brush Control in Southeastern New
York: Fifteen years of stable treeless communities. Ecology
34:63-73.
B-63
Probst, G.S., R.E. McMahon, L.E. Hill, C.Z. Thompson, J.K. Epp ,
and S.B. Neal. 1981. Chemiccdly induced unscheduled DNA
synthesis in primary rat hepatocyte cultures: A comparison with
bacterial mutagenicity using 218 compounds. Environmental
Mutagenesis. 3:11-32.
Quilty, S.P., and M.J. Geoghegan, 1976. University College, Ireland,
Private communication. As cited by TRW (1981) reference no. 23
on page A-168.
Ramsey, J.C., 1967. Tordon. Anal. Methods Pestic. Plant Growth
Regul., Food Additives 5: 507-25.
Ramsteiner, K.A., W. Hormann, and D. Eberle, 1972. Z.
Pflanzen-krankhelten. Sonderheft 6: 43. As cited by TRW (1981).
Rawls, C.K., 1965. Field tests of herbicide toxicity to certain
estuairine animsils. Chesapeake, Sci. , 6: 150-61.
Rawls, C.K., 1971. The accumulation and loss of field-applied
butoxyethanol ester of 2, 4-dichlorophenoxy acetic acid in eastern
oysters, Crassostrea virginica and soft-shelled clams, Mya
arenaria. Hyacinth Control J. 9: 62-78. As cited by NRCC
(1978).
Reed, Ellen H. , 1982. Vertical and lateral movement of residual soil
applied herbicides. Master's Thesis. Purdue University.
Regoli, A.J. and D.A. Laskowski, 1974. Aerobic Degradation of
14
Ring-labelled C-3,5,6-Trichloro-2-pyridyloxyacetic Acid in Soil.
Report No. GS-1364, April 17. As cited by TRW (1981).
Reuber, M.D. 1979. Carcinogenicity of 2 ,4-dichlorophenoxyacetic acid.
Frederick Cancer Research Center; Frederick, Maryland. 21701.
B-64
Reuber, M.D. 1981. Carcinogenicity of picloram. Journal of Toxicology
and Environmental Health. 7:207-22.
Rhodes, R.C., I.J. Belasio, and H.L. Pease, 1970. Determination of
mobility and adsorption of agrichemicals on soils. J. Agric. Food
Chem. 18: 524-8. As cited by Reed (1982).
Riccio, E.G. Shepherd, A. Poraeroy, K. Mortelmans, and M.D. Waters.
1981. Comparative studies between the S. cerevisiae D3 and D7
assays of eleven pesticides. Abstract no. P63 Environ. Mutagenesis
3(3):327.
Richards, N.A. 1973. Old field vegetation as an inhibitor of tree
vegetation. In Goodland, R. ed. Power Lines and the Environment,
proceedings of the CoUoquim "Biotic management along power
transmission rights-of-way" held at the American Institute of
Biological Sciences Annual Meeting Amherst, MA. June 21, 1973.
The Cary Arboretum of The New York Botanical Gardens.
Millbrook, N.Y. pp. 78-88.
Richter, 1952, See Pimentel (1971) bibliography. As cited by
Buffington (1974); (Richter, 1952, not included in bibliography).
Ritter, W.F., et al. Atrazine, propachlor, and diazinon residues on
small agricultural watersheds - Runoff losses, persistence and
movement. Environmental Science and Technology 8: 38-42. As
cited by TRW (1981).
Robens, 1978. As cited by Arthur D. Little, Inc. (1979); not included
in bibliography.
Rocchi, P. , P. Perocco, W. Alberghini A. Fini and G. Prodi. 1980.
Effect of pesticides on scheduled and unscheduled DNA synthesis
of rat thymocytes and human lymphocytes. Arch. Toxicol 45:101-8.
B-65
Rodgers, C. and D. Stalling, 1972. Dynamics of an ester of 2,4-D in
organs of 3 fish species. Weed Science 20(1): 101-5.
Roeth, F.W., T.L. Lavy, and O.C. Burnside, 1969. Atrazine
degradation in two soil profiles. Weed Science 17: 202. As cited
by TRW (1981).
Rogers, R.L., G.H. Willis, T.G. Hargroder, and J.L. Kilmer, 1974.
Losses of linuron and diuron in surface drainage water. Abstr.
1974. Meeting Weed Sci. Soc. of America, p. 56. As cited by
Reed (1982).
Rose, M.S. and L.L. Smith, 1977a. The Relevance of Paraquat
Accumulation by Tissues. Imperial Chemical Industries Limited,
Central Toxicology Laboratory, Alderley Park, Nr Macclesfield,
England, SKIO 4TJ.
Rose, M.S. and L.L. Smith, 1977b. Tissue uptake of paraquat and
diquat. Gen. Pharmacol. 8: 173-6.
Rose, M.S., L.L. Smith and I. Wyatt. 1980. Toxicology of herbicides
with Special reference to the bipyridiliums. Ann. Occup. Hyg.
23:91-4.
Rowe, V.K., and T.A. Hymas, 1954. Summary of toxicological
information on 2,4-D and 2,4,5-T type herbicides and an
evaluation of the hazards to livestock associated with their use.
Am. J. Vet. Res., 15: 622-9.
Rueppell, M.L. et al. , 1977. Metabolism and degradation of glyphosate
in soil and water. J. Agric. Food Chem. 25(3): 512-28. As cited
by TRW (1981).
Sachsse, K., 1973a. Skin Irritation in the Rabbit after Single
Application of Technical CGA-24705: Project No. Siss 2979. CDL:
B-66
112840-1. Unpublished study prepared by Ciba-Geigy, Ltd.,
Basle, Switzerland. As cited by EPA (1980).
Sachsse, K., 1973b. Irritation of Technical CGA-24705 in the Rabbit
Eye: Project No. Siss 2979. CDL: 112840-G. Unpublished study
prepared by Ciba-Geigy Ltd. , Basle, Switzerland. As cited by
EPA (1980).
Sachsse, K. and L. Ullman, 1974. Acute Inhalation Toxicity of
Technical CGA-24705 in the Rat: Project No. Siss 3516. CDL:
112840. Unpublished study prepared by Ciba-Geigy Ltd., Basle,
Switzerland. As cited by EPA (1980).
Salman, H.A., T.R. Bartley, and A.R. Hattrup, 1972. Progress
Report of Residue Studies on Dicamba Used for Ditchbank Weed
Control. USDI, REC-ERC-72-6. As cited by Velsicol Chemical
Corp. (1981).
Sanders, H.O., 1969. Toxicity of pesticides to the crustacean
Gammarus lacustris. Tech. Paper No. 25., USDI Bureau Sport
Fish. Wildl. As cited by NRCC (1978); EPA (1975).
Sanders, H.O., 1970a. Pesticide toxicity to tadpoles of the western
chorus frog, Pseudacris trisesiata, and Fowler's toad. Bufo
woodhoussi, fowler. Copeia, 2: 246-51. As cited by NRCC
(1978).
Sanders, H.O., 1970b. Toxicity of some herbicides to six species of
freshwater crustaceans. J. Water Pollut. Control Fed., 42:
1544-50. As cited by NRCC (1978); EPA (1975).
Sanders, H.O. and O.B. Cope, 1968. The relative toxicities of several
pesticides to naiads of three species of stoneflies. Limmol.
Oceanogr., 13: 112-7.
B-67
Sargent, M., et al. , 1971. The Toxicity of 2,4-D and Picloram
Herbicides to Fish. Purdue University and Indiana State Highway
Commission, NTIS PB-20 1-099, February 1971, 22 pp. As cited by
TRW (1981).
Schlapfer, T.A., 1977. Environmental Impact Statement: Vegetation
Management with Herbicides. USDA-FS-R6-DES(ADM)75-18. USDA
Forest Service, Portland, Oregon, 668 pp. As cited by TRW
(1981).
Schultz, D.P., 1973. Dynamics of a salt of 2,4-D in fish, water, and
hydrosol. J. Agr. Fd. Chem. 21: 186-92.
Schultz, D.P. and P.D. Harman, 1974. Residues of 2,4-D in pond
waters, mud, and fish, 1971. Pestic Monit. J. 8: 173-9. As cited
by NRCC (1978).
Schultz, D.P. and E.W. Whitney, 1974. Monitoring 2,4-D residues at
Loxahatchee National Wildlife Refuge. Pestic. Monit. J. 7: 146-52.
And as cited by NRCC (1978).
Schwartz, H.G., Jr., 1967. Microbial degradation of pesticides in
aqueous solutions. J. Water. Poll. Control. Fed. 39(10): 1701-16.
As cited by TRW (1981).
Schwetz, B.A., J.M. Norris, G.L. Sparschu, V.K. Rowe, P.J.
Gehring, J.L. Emerson, and C.G. Gerbig, 1973. Toxicology of
chlorinated dibenzo-p-dioxins. Environ. Health Perspec. 5: 87-99.
Scott, D.C., and J.B. Weber, 1967. Herbicide phytotoxicity as
influenced by adsorption. Soil Science 104: 151. As cited by
Simsiman, et al. (1976).
Scott, H.D. and J.F. Lutz , 1971. Release of herbicides from clay
minerals as a function of water content: I. kaolinite, Proc. Soil
Sci. Soc. Am. 35: 374-9. As cited by NRCC (1978).
B-68
Scribor, G. , 1977b. Report to Ciba-Geigy Corporation: Primary Skin
Irritation Test with Dual 8E in Albino Rabbits: IBT No.
8530-10822. CDL: 232191-E. Unpublished study prepared for
Ciba-Geigy Corp., Greensboro, N.C. As cited by EPA (1980).
Scrifres, C.J., and T.J. Allen, 1973. Dissipation of dicamba from
grassland soils of Texas. Weed Sci. 21(5): 393-6. As cited by
TRW (1981).
Seiler, J. P. 1977. Nitrosation in vitro and in vivo by sodium nitrate,
and mutagenicity of nitrogenous pesticides. Mutation Research
48:225-36.
Seiler, J. P. 1978. Herbicidal phenylalkylureas as possible mutagens. I.
Mutagenicity tests with some urea herbicides. Mutation Research.
58:353-9.
Selypes, A., L. Nagymajtenyi, and G. Berencsi. 1980. Mutagenic and
embryotoxic effects of paraquat and diquat. Bull. Environm.
Contam. Toxical. 25:513-7.
Serdy, F. , 1980. Personal Communication with M. Ghassemi of TRW on
June 18. As cited by TRW (1981), reference no. 20 on page
A-168.
Shearer, R.W. 1974. Specificity of chemical modification of ribonucleic
acid transport by liver carcinogens in rat. Biochemistry
13(8):1764-7.
Sheets, T.J., 1961. Persistence of Herbicides in Soil. Agricultural
Research Services, USD A, Beltsville, MD As cited by TRW
(1981).
Sheets, T.J. 1964. Metabolism of herbicides: Review of disappearance
of substituted urea herbicides from soil. Agricultural and Food
Chemistry 12(1): 30-3.
B-69
Sheets, T.J., 1970. Persistence of triazine herbicides in soils.
Residue Reviews 32: 287-310. As cited by TRW (1981).
Sheets, T.T., and V.F. Lutz , 1969. Bull. N.C. Exp. Sta, As cited
by J.E. Johnson, (1971), no title provided.
Sherman, H., 1979. Toxicological Information: Fosamine Ammonium
Salt, Ammonium Ethyl Carbamoylphosphonate. Unpublished report
by Haskell Laboratory for Toxicology and Industrial Medicine, E.I,
du Pont de Nemours and Company, Wilmington, DE
Sherman, H. and A.M. Kaplan, 1975. Toxicity studies with
5-bromo-3-sec-butyl-6-methyluracil. Toxicology and Applied
Pharmacology 34(2): 189-96.
Sherman, H. and E.F. Stula, 1965. Toxicity studies on ammonium
sulfamate. Toxicol. Appl. Pharmacol. 7: 497.
Sherman, H. and E.F. Stula. 1966. Pathology Report: Ammonium
Sulfamate. Unpublished report by Haskell Laboratory for
Toxicology and Industrial Medicine, E.I. duPont de Nemours and
Company.
Shirasu, Y., M. Moriya, K. Kato, A. Furahashi, and T. Kada. 1976,
Mutagenicity screening of pesticides in the microbial system.
Mutation Research 40:19-30.
Sikka, H.C., H.T. Appleton, and E.O. Gangstad, 1977. Uptake and
metabolism of dimethylamine salt of 2,4-dichlorophenoxyacetic acid
by fish. J. Agric. Food Chem. 25: 1030. As cited by Gangstad
(1982).
Simmons, V.F., D.C. Poole and G.W. Newell. 1976. In vitro mutagenic
studies of twenty pesticides. Abstract no. 42. Toxicol. Appl.
Pharmacol. 37:109.
B-70
Simmons, V.F., D.C. Poole, E.S. Riccio, D.E. Robinson, A.D.
Mitchell, M.D. Waters, 1979. In vitro mutagenicity and
genotoxicity assays of 38 pesticides. Abstract No. Ca-9.
Environ. Mutagenesis 1:142-3.
Simsiman, G.V., and G. Chesters, 1975. Persistence of diquat in the
aquatic environment. Water Res. Accepted for publication. As
cited by Simsiman, et al. (1976).
Simsiman, G.V., T.C. Daniel and G. Chesters, 1976. Diquat and
endothall: Their fates in the environment Residue Rev. 62:
131-74.
Sirons, G.., R. Frank and R. Dell. 1977. Picloram residues in sprayed
Macdonald-Cartier Freeway right-of-way Bulletin of Environmental
Contamination and Toxicology. 18:526-32.
Skipper, H.D., B.J. Gossett, and G.W. Smith, 1976. Field Evaluation
and soil residual characteristics of CGA-24705 and Alachlor.
Proceedings of the Twenty-Ninth Annual Meeting of the Southern
Weed Science Society; Jan. 27-29, 1976, Dallas, TX. Raleigh,
N.C. Southern Weed Science Society, pp. 418-422. As cited by
EPA (1980).
Slade, P., 1965. Photochemical degradation of paraquat. Nature 207:
515. As cited by Simsiman, et al. (1976).
Slade, P. , 1966. The fate of paraquat applied to plants. Weed
Research 6: 158. As cited by Simsiman, et al. (1976).
Slade, P., and A.E. Smith, 1967. Photochemical degradation of diquat.
Nature 213: 919. As cited by Simsiman, et al. (1976).
Slodki, M.E., and L.J. Wickerham, 1966. Extracellular polysaccharides
and classification of the genus Lipomyces J. Gen. Microbiol. 42:
381. As cited by Simsiman, et al. (1976).
B-71
Smith, A.E., 1972. The hydrolysis of 2,4-dichlorophenoxyacetate I
esters to 2,4-dichlorophenoxyacetic acid in Saskatchewan soils.
Weed Res. 12: 364-72. As cited by NRCC (1978).
Smith, A.E., 1973. Degradation of dicamba in prairie soils. Weed Res.
13: 373-8. As cited by TRW (1981).
Smith, A.E., 1974. Breakdown of herbicide dicamba and its
degradation product, 3 ,5-dichlorosalicylic acid in prairie soils. J.
Agric. Food Chem. 22(4): 601-605. As cited by TRW (1981).
Smith, A.E., 1975. Field persistence studies with herbicides in prairie
soils. In: Coulston, F. and F. Korte, eds. Environmental Quality
and Safety Suppl. v. 3 lUPAC 3rd Int. Congress, pp. 266-70. As
cited by NRCC (1978).
Smith, A.E., 1976. The hydrolysis of herbicidal phenoxyalkanoic esters
to phenoxyalkanoic acids in Saskatchewan soils. Weed Res. 16: d
19-22. As cited by NRCC (1978). '
Smith, A.E., and D.R. Cullimore, 1975. Microbiological degradation of
the herbicide dicamba in moist soils at different temperatures.
Weed Res. 15: 59-62. As cited by TRW (1981).
Smith, A.E., R. Grover, G.S. Emmond, and H.C. Korven, 1975.
Persistence and movement of atrazine, bromacil, monuron, and
simazine in intermittently-fiUed irrigation ditches. Can. J. Plant
Sci. 55: 809-16. As cited by Reed (1982).
Smith, G.E. and D.G. Isom, 1967. Investigation of effects of large
scale applications of 2 , 4-D on aquatic fauna and water quality .
Pestic. Monit. J. 1(3): 16-21. As cited by NRCC (1978); USDA
(1973).
B-72
Smith, J.W. and T.J. Sheets. 1967. Uptake, distribution, and
metabolism of monuron and diuron by several plants. J. Agr.
Food Chem. 15:577-581.
Smith, K.S., 1977. Report: Catfish Bioaccumulation Study Following
14
Exposure to C-Metolachlor in a Soil/ Water /Fish Ecosystem.
7E-6506; Received Feb, 6, 1978 under 100-583. CDL: 232789-U,
Unpublished study prepared by Cannon Laboratories, Inc. for
Ciba-Geigy Corp., Greensboro, N.C. As cited by EPA (1980).
Smith, R.J., Jr. and W.B. Ennis, Jr., 1953. Studies on the downward
movement of 2,4-D and 3-chloro-IPC in soils. Proc. South. Weed
Conf. 6: 63-71. As cited by NRCC (1978).
Smith, S.H.; G.L. Adler, 1978. Final Report to Ciba-Geigy
Corporation: Three-Generation Reproduction Study with
CGA-24705 Technical in Albino Rats: IBT No. 8533-07928. CDL:
96718-A; 96718-B; Ciba-Geigy Corp., Greensboro, N.C. As cited
by EPA (1980).
Solt, Aik. and S. Neale. 1980. Induction of bacterial mutations by
mutagenic metabolites produced in intact mice. Abstract no. 90.
Mutation Research 74(3): 214.
Somers, J.D., E.T. Moran, B.S. Reinhart, and G.R. Stephenson, 1972.
Effect of external application of pesticides to the egg of the hen
and pheasant on hatchability and chick viability. Poult. Sci. 51:
1862. As cited by NRCC (1978).
Somers, J.D., E.T. Moran and B.S. Reinhart, 1974a. Effects of
external application of pesticides to the fertile egg on hatching
success and early chick performance. 2. Commercial herbicide
mixtures of 2,4-D with Picloram or 2,4,5-T using the pheasant.
BuU. Environ. Contam. Toxicol., 11: 339-42.
B-73
Somers, J.D., E.T. Moran and B.S. Reinhart, 1974b. Effect of
external application of pesticides to the fertile egg on hatching
success and early chick performance. 3. Consequences of
combining 2,4-D with picloram and extremes in contamination.
Bull. Environ. Contam. Toxicol, 11: 511-6.
Somers, J.D., E.T. Moran, B.S. Reinhart and G.R. Stephenson, 1974c.
Effect of external application of pesticides to the fertile egg on
hatching success and early chick performance. 1. Preincubation
spraying with DDT and commercial mixtures of 2,4-D: Picloram
and 2,4-D: 2,4, 5-T. Bull. Environ. Contam. Toxico. , 11: 33-8.
Sonnet, P.E., 1979. Toxicity of pesticide combinations and pesticide
metabolic products to honeybees. Abstract USDA-ARS Bee District
Laboratory, Laramie, WY May 1979. As cited by TRW (1981).
Sorrie, B.A., 1983 (April). Rare Vascular Plant Species in
Massachusetts. Massachusetts Natural Heritage Program, Dept. of
Environmental Management, Boston, MA.
Sorsa, M. and U. Gripenberg. 1976. Organization of mutagenicity test
system combining instructive purposes: testing for mutagenic
effects of the herbicide "amitrole". Abstract, no. 53. Mutation
Research 38:132-3.
Sosnovskaya, E.A. and P.D. Pashchenko, 1965. The effect of
herbicides on microflora of the soil under maize. Proc. VI Conf.
Chemicalization Agric. pp. 179-82. (Weed Abstr. 16: 184, 1967)
As cited by TRW (1981).
Sparschu, G.L. F.L. Dunn and V.K. Rowe. 1971. Study of the
teratogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in the rat.
Ed. Cosmet. Toxicol. 9:405-12.
Sprankle, P. , et al, 1975. Rapid inactivation of glyphosate in the soil.
Weed Science 23(3): 224-8. As cited by TRW (1981).
B-74
i
Spurrier, E.G. 1973. Glyphosate-A new broad-spectrum herbicide.
PANS 19(4):607-12.
Squire, R.A. and M.H. Levitt, 1975. Report of a workshop on
classification of specific hepatocellular lesions in rats. Cancer
Research 35:3214-5.
St. John, L.E., Jr. and D.J. Lisk, 1969. Metabolism of Banvel-D
herbicide in a dairy cow J. Darby Sci., 52(3): 392-3.
Stalling, D. and J. Huckins, 1978. Metabolism of 2,4-D in bluegills and
water. J. Agr. Fd. Chem. 26(2): 447-52.
Steenson, T.I. , and N. Walker, 1957. The pathway of breakdown of
2 , 4-dichloro- and 4-chloro-2-methyl phenoxyacetic acid by
bacteria. Journal of General Microbiology 16: 146-54. As cited by
USDA (1973).
Steenson, T.I., and N. Walker, 1958. Adaptive patterns in the
bacterial oxidation of 2, 4-dichloro and 4-chloro-2-methyl-phenoxy-
acetic acid. Journal of General Microbiology 18: 692-7. As cited
by USDA (1973).
t
Stevens, M.A., and J.K. Walley, 1966. Tissue and milk residues
arising from ingestion of single doses of diquat and paraquat by
cattle. J. Sci. Food Agr. 17: 472. As cited by Simsiman, et al.
(1976).
Stewart, D.K.R. and S.O. Gaul, 1977. Persistence of 2,4-D, 2,4,5-T
and dicamba in Dykeland soil. Bull. Environm. Contam. and Tox.
18 No. 2: 210-218. As cited by Velsicol Chemical Corp. (1981).
Stupnikov, A. A., 1972. Comparative toxicity of butyl esters 2,4-D and
2,4,5-T used in the form of an aqueous emulsion and in mineral oil
solution for some species of mammals and wildfowl. Vliyanie
Pestits, Dikikh Zhivoth. , pp. 121-4. As cited by NRCC (1978).
B-75
Sund, K., 1956. Residual activity of 3-amino-l,2,4-triazole in soils. I
J. Agr. Food Chem. 4(1): 57-60, 1956. As cited by TRW (1981).
Surber, E.W., and Q.H. Pickering, 1962. Acute toxicity endothall,
diquat, thyamine, dalapon, and silvex to fish. Prog.
Fish-Culturist 24: 164. As cited by Simsiman, et al. (1976).
Suschetet, M., and J. Causeret, 1973. Toxicologie et nutrition.
Effects physiopathologiques et nitritionels de I'acide amino-4
trichloro-3,5,6 picolinique (piclorame) chez le rat. [Physiopatho-
logical and nutritional effects of 4-amino-3,5,6-trichloropicolinic
acid (picloram) in the rat.] C.R. Acad. Sc. Paris 276: 1775-7.
Series D. As cited by Arthur D. Little, Inc. (1979).
Suschetet, M. , J. LeClerc, M. Lhuissier, and W. Loisel, 1974. Toxicite
et effects nutritionels chez le rat, de deux herbicides: Le
piclorame (Acide amino-4 trichloro-3,5,6 picolinique) et I'atrazine
(Chloro-2 ethylamino-4 isopropylamino-6-s-triazine) . [Toxicity and a
nutritional effects in the rat, of two herbicides: Picloram (4-amino-
3,56-trichloropicolinic acid) and atrazine (2-chloro-4-ethylamino-6-
isopropylamino-S-triazine) ] Ann. Nutr. Alim. 28: 29-47, As cited
by Arthur D. Little, Inc. (1979).
Svenson, H.A. 1966. Vegetation Management for Rights-of-Way .
Eastern Region, Forest Service, USD A.
Swabey, Y.H., and C.F. Schenk, 1963. Algicides and aquatic
herbicides. Proc. 3rd Ann. Meeting Aq. Weed Control Soc. , pp.
1-20. As cited by Simsiman, et al. (1976).
Swan. F.R. 1970. Post-fire response of four plant communities in
south-central New York state. Ecology 51:1075-82.
Swanson, C.R. and W.C. Shaw, 1954. The effect of
2 , 4-dichlorophenoxyacetic acid on the hydrocyanic acid and nitrate
B-76
content of sudan grass. Agron J. 46: 418. As cited by USD A
(1973).
Tarrant, B.F. and L.A. Norris, 1967. Residues of herbicides and
diesel oil carriers in forest waters: A review. In: Symposium
Proceedings: Herbicide and Vegetation Management in Forests,
Ranges, and Noncrop Lands, Oregon State Univ. As cited by
TRW (1981).
Taylor, H.F., and R.L. Wain, 1962. Side-chain degradation of certain
phenoxyalkane carboxylic acid by Nocardia coeliaca and other
micro-organisms isolated from soil. Proceedings of the Royal
Society of London, Series B, 156: 172-86. As cited by USD A
(1973).
Teater, R.W., J.L. Mortensen and P.F. Pratt, 1958. Effect of certain
herbicides on rate of nitrification and carbon dioxide evolution in
soil, J. Agr. Fd. Chem. 6: 214-6.
Thompson, B.F. 1977. The Changing Face of New England. Houghton
Mifflin. Co. , Boston, MA.
Thompson, P.J., J.L. Emerson, R.J. Strebing, C.G. Gerbig and V.B,
Robinson. 1972. Teratology and postnatal studies on
4-amino-3,5,6,-tri-chloropicolinic acid (picloram) in the rat. Ed.
Cosmet. Toxicol. 10:797-803.
Thomson, W.T., 1975. Agricultural Chemicals. Book II Herbicides
1975-76 Revision. Thomson Publications, Fresno, CA
Tietjen, H.P., 1973. 2,4-D, vegetation, and pocket gophers. Colorado
State Univ. Exp. Stn. Bull. 5545: 63-71. As cited by NRCC
(1978).
Tillman. R. 1976. The southern tier interconnection: A case study.
In Tillman, R.ed. Proc. First National Symposium on Environmental
B-77
Concerns in Rights-of-Way Management. Mississippi State i
University, pp. 221-30.
Torgeson, D.C., and H. Mee, 1967. Microbial degradation of bromacil.
Proc. NEWCC, p. 584-5. As cited by HiU (1971).
Torracca, A.M., G. Gardamone, V. Ortali, A. Carere, R. Raschetti,
and G. Ricciardi, 1976. Mutagenicity of pesticides as pure
compounds and after metabolic activation with rat inner
microsomes. Atti. Assoc. Genet. Ital. 21: 28-9.
Trichell, D.W., H.L. Morton, and M.G. Merkle, 1968. Loss of
herbicides in runoff water. Weed Sci. 16(4): 447-9. As cited by
TRW (1981).
Triplett, G.B., et al, 1978. Transport of atrazine and simazine in
runoff from conventional and no-tillage corn. J. Environ. Quality
7(1): 77. As cited by TRW (1981). a
TRW. 1981. Environmental Fates and Impacts of Major Forest Use
Pesticides. USEPA. Office of Pesticides and Toxic Substances.
Contract No. 68-02-3174. , Washington, D.C.
Tsuda, H., M. Hananouchi, M. Tatematsu, M. Hirose, K. Hirao, M.
Takahashi, and N. Ito. 1976. Tumorigenic effect of
3-amino-l,2,4-triazole on rat thyroid. J. Natl. Cancer Inst.
57(4):861-3.
Tu, CM., 1966. Interaction between Dipyridylium Herbicides and
Microbes, in Soil. Ph.D. Thesis. Oregon State University,
Corvallis, Oregon. As cited by Simsiman, et al. (1976).
Tu, CM., and W.B. Bollen, 1969. Effect of Tordon herbicides on
microbial activities in three Willamette Valley soils. Down to Earth
25(2): 15-7. As cited by USDA (1973).
i
B-78
Tucker, B.V., D.E. Pack, and J.N. Ospenson, 1967. Adsorption of
bipyridylium herbicides in soil. J. Agric. Food Chem. 15: 1005.
As cited by Simsiman, et al. (1976).
Tucker, R.K. and D.G. Crab tree, 1970. Handbook of Toxicity of
Pesticides to Wildlife Bureau of Sport Fisheries and Wildlife.
Bureau of Sport Fisheries and Wildlife Denver Wildlife Research
Center, Resource Publication No. 84.
Tye, R. and D. Engel, 1967. Distribution and excretion of dicamba by
rats as determined by radio tracer-technique J. Agr. Fd. Chem.,
15: 837-40.
U.S. Department of Interior, 1978. Final Environmental Statement.
Vegetation Management with Herbicides; Western Oregon. Volume
I, Chapter 3. USDI, Bureau of Land Management, Washington,
D.C.
U.S. Department of Interior, FWPCA, 1968. Water Quality Criteria,
Report of the National Technical Advisory Committee to the
Secretary of the Interior. 234 pp. As cited by EPA (1975).
U.S. Forest Service, 1974. Region 6, Vegetation Management with
Herbicides Environmental Impact Statement, U.S. Dept. of
Agriculture, Britland, OR. As cited by USDOE (1980).
Unger, T.M., J. Kliethermes, D. VanGoethem, and R.D. Short, 1981.
Teratology and Postnatal studies in rats of the propylene glycol
butyl ether and isooctyl esters of 2 ,4-dichlorophenoxyacetic acid.
US NTIS PB Rep. P B81-191, 140: 27pp.
Union Carbide, 1977. Material Safety Data Sheet for Weedar 64, DMA
Salt of 2,4-D. Salinas, California
B-79
University of California, 1975. Toxicity of Pesticides to Honey Bees. i
Leaflet 2286. U.C., Division of Agricultural Sciences, Riverside,
CA As cited by TRW (1981).
Upchurch, R.P. and D.D. Mason, 1962. The influence of soil organic
matter on the phytotoxicity of herbicides. Weeds 10: 9-14. As
cited by NRCC (1978).
USD A. 1973. Herbicide Use in Mt. Hood, Rogue River and Willamette
National Forests. Final Environmental Impact Statement.
USD A, 1977. Final Environmental Statement Vegetation Management with
Herbicides in the Eastern Region. USDA-FSR9 FES ADM-77-10.
As cited by TRW (1981).
USD A, 1978. Final Environmental Statement: Vegetation Management
with Herbicides. USDA-FS-R6-FES (ADM) 75-18, USDA, Pacific
Northwest Region, Forest Service, Portland, OR. p. 132-3. As ^
cited by TRW (1981). '
USDOE, 1980. BonneviUe Power Administration; 1981 Construction and
Maintenance, Final Environmental Impact Statement.
U.S. D.O.I. 1980. Management of Transmission Line Rights-of-Way for
Fish and Wildlife. Volumes 1 and 2. FWS/OBS-79/22.
Vainio, H, J. Nickels, and K. Linnainmaa. 1982. Phenoxyacid
herbicides cause peroxisome proliferation in Chinese Lamsters.
Scand. J. Work Environ. Health 8(1): 70-3.
Van der Bosch, R. , P.S. Messenger, and A. P. Gutierrez. 1982. An
Introduction to Biological Control. Plenum Press, New York.
Van Deuren, B.L. and B.M. Goldschmidt. 1976. Cocarcinogenic and
tumor-promoting agents in tobacco carcinogenesis. J. Natl. Cancer
Inst. 56(6): 1237-42. ^
B-80
Velsicol Chemical Corp., 1974a. Banvel Herbicide General Bulletin. No.
521-2. As cited by USDA (1973); TRW (1981).
Velsicol Chemical Corp., 1974b. Banvel Environmental Impact Statement
Outline, Chicago, XL As cited by USDOE (1980).
Velsicol Chemical Corp., 1981. The Herbicide Dicamba: A Survey of
its Action, History, Worldwide Registration Status, Chemistry,
Environmental /Fate and Effects, and Toxicity to Terrestrial and
Aquatic Organisms, Chicago, IL.
Vettorazzi, G. , 1975. State of the art of the toxicological evaluation
carried out by the Joint FAO/WHO Expert Committee on Pesticide
Residues. I. Organohalogenated pesticides used in public health
and agriculture. Residue Review 56: 107-34.
Vigfusson, N.V. and E.R. Vyse. 1980. The effect of the pesticides,
Dexon, Captan and Roundup, on sister-chromatid exchanges in
human lymphocytes in vitro. Mutation Research 79:53-7.
Vilkas, A.G., 1976. Acute Toxicity of CGA-24705 Technical to the
Water Flea Daphnia magna. Received November 23, 1976 under
100-587. CDL: 226955-C, Unpublished study prepared by Aquatic
Environmental Sciences, Union Carbide Corp. for Ciba-Geigy
Corp., Greensboro, N.C. As cited by EPA (1980).
Vivier, P. and M. Nisbet, 1965. Toxicity of Some Herbicides,
Insecticides, and Industrial Wastes, p. 167-9. In: Biological
Problems in Water Pollution. Third Sem. , 1962 U.S. Pub. Heal.
Serv. Publ. 999-WP-25. As cited by TRW (1981).
Volts, T.P., et al. , 1974. Soil microbiological and biochemical effects
of long term atrazine applications. Soil Biology and Biochemistry
6(1): 149-52. As cited by TRW (1981).
B-81
Von Rumker, O., E.W. Lawless, and A.F. Meiners, 1975. Production m
Distribution, Use and Environmental Impact Potential of Selected
Pesticides. EPA 540/1-74-001. U.S. EPA, Office of Pesticide
Programs, Washington, D.C., pp. 211-7. As cited by TRW
(1981).
Wahlenberg, W.G. and W.T. Doolittle. 1950. Reclaiming Appalachian
brushlands for economic forest production. J. For. 48:170-4.
Walker, C.R., 1962. Toxicological effects of herbicides on the fish
environment. Ann. Air Water Poll. Conf. (November 12, Columbia,
MO), Proc. 8: 17-34. As cited by TRW (1981).
Walker. C.R., 1964. Simazine and other s-triazine compounds as
aquatic herbicides in fish habitats. Weeds, 12(2): 134-9.
Walker, E.M., Jr., G.R. Gale, L.M. Atkins and R.H. Gadsden. 1979.
Some effects of atrazine on Ehrlich ascites tumor cells in vitro and M
in vivo Bull. Environm. Contam. Toxicol. 22:095-102. ^
Warren, S. and W.A. Wiering. 1973. Soil moisture studies in relation to
prescribed burning of fields and forest. Ecol. Soc. Amer. Bull.
54:21.
Washington State University and Department of Agriculture, 1971.
Washington Pest Control Handbook. Washington State University,
Pullman, Washington, 569 pp. As cited by USDA (1973).
Watson, J.R., 1977. Seasonal variation in the biodegradation of 2,4-D
in river water. Water Res. 11(2): 153-7. As cited by TRW
(1981).
Weber, J.B., and H.D. Coble, 1968. Microbial decomposition of diquat
adsorbed on montmorillonitic and kaolinitic clays. J. Agric. Food
Chem. 16: 475. As cited by Simsiman, et al. (1976).
4
B-82
Weber, J.B., and S.B. Weed, 1968. Adsorption and desorption of
diquat, paraquat, and prometone by montmorillonitic and kaolinitic
clay minerals. Soil Sci. Soc. Amer. Proc. 32: 485. As cited by
Simsiman, et al. (1976).
Weber, J.B., P.W. Perry, and R.P. Upchurch, 1965. The influence of
temperature and time on the adsorption of paraquat, diquat,
2,4-D, and prometone by clays, charcoal, and an anion-exchange
resin. Soil Sci. Soc. Amer. Proc. 29: 678. As cited by Simsiman,
et al. (1976).
Weed, S.B., and J.B. Weber, 1969. The effect of cation exchange
capacity on the retention of diquat and paraquat by three-layer
clay minerals. I. Adsorption and release. Soil Sci. Soc. Amer.
Proc. 33: 379. As cited by Simsiman, et al. (1976).
Weir. R.J., O.E. Daynter and J.R. Elsea, 1958. Toxicology of
3-amino-l,2,4-triazole. Hormolog, 2(2): 13-4.
Wellborn, T.L., Jr., 1969. ' The toxicity of nine therapeutic and
herbicidal compounds to striped bass. Progressive Fish-Culturist
31: 27. As cited by Simsiman, et al. (1976).
Whitehead, C.C., and R.J. Pettigrew, 1972. The subacute toxicity of
2,4-dichlorophenoxyacetic acid and 2,4,5-trichlorophenoxyacetic
acid to chick. Toxicol. Appl. Pharmacol. 21: 348-54. As cited by
NRCC (1978).
Whitney, E. , R. Estes, R. Smitherman and E. Gangstad, 1974. Effects
of silvex on aquatic biota. Hyacinth Control J., 12: 20-4.
Wiering, W.A. and F.E. Egler 1955. A shrub community of Viburnum
lentago, stable for twenty-five years. Ecology 36: 356-60.
B-83
Wiese, A.F. and R.G. Davis, 1964. Herbicide movement in soil with
various amounts of water. Weeds 12: 101-3. As cited by TRW
(1981).
Wilbert, D.E., 1963. Some effects of chemical sagebrush control on elk
distribution. J. Range Manage., 16: 74-8.
Wildeman, A.G. and R.N. Nazar 1982. Significance of plant metabolism
in the mutagenicity and toxicity of pesticides. Can J. Genet.
Cytol. 24:437-49.
Willard, C.J., 1950. Indirect effects of herbicides. Proc. 7th N.
Central Weed Control Conf. p. 110. As cited by USDA (1973).
Williams, C.S., 1971. Tordon 22K safety to livestock. Mimeographed
letter from Dow Chemical Company dated July 16, 1971. As cited
by K.L. Carvell (1973).
Willis, G.H., R.I. Rogers, and E.M. Southwick, 1975. Losses of
diuron, linuron, fenac, and trifluralin in surface drainage water.
J. Envir. Qual. 43(3): 399-402. As cited by Reed (1982).
Wilson, D.C., and C.E. Bond, 1969. The effect of the herbicides
Diquat and dichlobenil (casoron) on pond invertebrates. Part 1.
Acute toxicity. Trans. Amer. Fish. Soc. 98: 438. As cited by
Simsiman, et al, (1976).
Wilson, R.G., Jr. and H.H. Cheng, 1976. Breakdown and movement of
2,4-D in the soil under field conditions. Weed Sci. 24(5): 461-6.
As cited by TRW (1981).
Witt, J.S., and D.M. Baumgartner, 1979. A Handbook of Pesticide
Chemicals for Forest Use. Forest Pesticide Shortcourse,
Washington State University and Oregon State University, pp.
9-10. As cited by TRW (1981).
I
B-84
Wojtalik. T., T. Hall and L. Hill, 1971. Monitoring ecological conditions
associated with wide-scale applications of DNA 2,4-D to aquatic
environments, Pestic, Monit, J., 4: 184-203.
Wolfe, N.L., et al. , 1976. Chemical and Photochemical Transformation
of Selected Pesticides in Aquatic Systems. EPA-600/ 3-76-067, U.S.
EPA, Environmental Research Laboratory, Athens, Georgia, pp.
125-8. As cited by TRW (1981).
Woodward, D.F., 1976. As cited by Arthur D. Little, Inc. (1979); not
included in bibliography.
Woodward, D.F., 1979. Assessing the hazard of picloram to cutthroat
troat. Journal of Range Management 32(3): 230-2, As cited by
Arthur D. Little, Inc. (1979), TRW (1981).
Woodward, D.F. and F.L. Mayer, Jr., 1978. Toxicity of three
herbicides (butyl, isooctyl, and propylene glycol butyl ether
esters of 2,4-D) to cutthroat trout and lake trout. Technical
Paper vol. 97 U.S. Fish and Wildlife Service, Columbia, Nat.
Fish. Res. Lab., Jackson, WY
Yeo, R.R., 1967. Dissipation of diquat and paraquat and effects on
aquatic weeds and fish. Weeds 15: 42. As cited by Simsiman, et
al. (1976).
Yoder, J., M. Watson, and W.W. Benson 1973. Lymphocyte chromosone
analysis of agricultural workers during extensive occupational
exposures to pesticides. Mutation Research 21:335-40.
Yoshida, K. and Yasuhiro Nishiuchi, 1972. Toxicity of pesticides to
some water organisms. Bull. Agr. Chera. Inspect. Stn. 12: 122-8.
Young, A.L.; E.L. Arnold, and A.M. Wachinski, 1974. Field studies of
the soil persistence and movement of 2,4-D, 2,4,5-T, and TCDD.
B-85
Abstract No. 226. Presentation to Weed Sci. Soc. Am. Las Vegas,
NV As cited by NRCC (1978).
Young, H.E. and D.B. Hatton. 1983. Right-of-way Forestry.
Manuscript, presented during the Transportation Research Board
Annual Meeting, January 1983.
Youngson, C.R., et al, 1967. Factors influencing the decomposition of
Tordon herbicide in soils. Down to Earth 23: 3-8,10-11. As cited
by TRW (1981).
Yu, C.C., D.J. Hansen, and G.M. Booth, 1975. Fate of dicamba in a
model ecosystem. Bull. Environ. Contam. Toxicol. 13(3): 280-3.
As cited by Velsicol Chemical Corp. (1981).
Zaccaro, L. , A. Abbondandalo and S. Bonatti. 1980. Results of
mutagenicity tests on the herbicide atrazine. Abstract no. 161.
Mutation Research 73.
Zepp, R.G., N.L. Wolf, J. A. Gordon, G.L. Baughman, 1975. Dynamics
of 2,4-D esters in surface waters: hydrolysis, photolysis, and
vaporization. Environ. Sci. Technol. 9: 1144-50. As cited by
TRW (1981).
Zetterberg, G., L. Busk, R. Elovson, I. Starec-NordenLamme and H.
Ryttman, 1977. The influence of pH on the effects of 2,4-D
( 2, 4-dichlorophenoxy acetic acid, Na Salt) on Saccharomyces
cerevisiae and Salmonella typhimurium. Mutat. Res. 42: 3-18.
Zick, W.H. and T.R. Castro, 1966. Dicamba — dissipation in and on
living plants. Proc. Brit. Weed Control Conf. 8th, pp. 265-265d.
As cited by Arthur D. Little, Inc. (1979).
Zilkah, S., M.E. Osband and R. McCaffrey. 1981. Effect of inhibitors
of plant cell division on mammalian tumor cells in vitro. Cancer
Research 41:1879-83.
B-86
4
Zimakowska, D. , 1973. Effects on 2,4-D-Na of various concentrations
on respiration of an aquatic crustacean Ascellus aquaticus. L.
Pol. Arch. Hydrobiol., 20: 469-73
Zimdahl, R.L., et al, 1970. Weed Research 10: 18. As cited by TRW
(1981), no title provided.
B-87
I
i
i
3625 01*6
V
\
I
i
1
\
ACME
BOOKBINDING CO., INC.
yUN 25 1987
100 CAMBRIDGE STREET
CHARLESTOWiM. MASS.
\